First blog post in a while, as most content now goes via Patreon (link on the homepage). In Reading this article, please be aware that it is not denying Covid-19, although I prefer to focus upon SARS-CoV-2 as a specific viral strain rather than a collection of symptoms classed a disease.

This article focuses upon the vaccine trials which have not set out to prove efficacy in preventing mortality or viral transmission, and on the reactionary "science" that broke out as the pandemic unfolded and has not been updated as things became clearer.


Product Type: Vaccine 
Item Code (Source): NDC: 59267-1000
Administration: Intramuscular

Ingredients: RNA ingredient BNT-162B2 (UNII: 5085ZFP6S) (RNA ingredient BNT-162B2 - UNII:5085ZFP6S)

Basis of Strength: RNA ingredient BNT-162B2
Strength: 0.23 grams in 1.8 millilitres 

lipid ALC-0159 (UNII: PJH39UMU6H)
lipid ALC-0315 (UNII: AVX8DX713V)
POTASSIUM CHLORIDE (UNII: 660YQ98I10)
MONOBASIC POTASSIUM PHOSPHATE (UNII: 4J9FJ0HL51)
SODIUM CHLORIDE (UNII: 451W47IQ8X)
SODIUM PHOSPHATE, DIBASIC, UNSPECIFIED FORM (UNII: GR686LBA74)
SUCROSE (UNII: C151H8M554)

The Covid-19 pandemic created an immediate discussion regarding the prospects for vaccination against the virus responsible for the cluster of symptoms classified as Covid-19, the now infamous SARS-CoV-2. Researchers around the globe working for various research institutions and pharmaceutical companies began work, much early research was based upon prior work regarding unsuccessful SARS vaccines. Throughout the Spring, Summer and beyond “experts” and government ministers promised, that if all goes well, an “effective” vaccine may be achieved by *insert various dates here.*

SARS-CoV-1 or severe acute respiratory syndrome referred to as SARS had approximately 100 cases in the United Kingdom, out of 8096-8422 total cases globally, and no deaths in the United Kingdom. The United Kingdom had 31 cases of MERS-CoV of a total of 2449 and two deaths in. the United Kingdom. Globally at least 774-916 deaths occurred (1), giving a case fatality rate of 11 per cent (2), which in theory suggest it to be highly lethal. Despite this, it seemingly mysteriously vanished. Coronaviruses, as previously discussed, are a large family of viruses, ranging from the common cold to more severe diseases, including the novel coronaviruses, including SARS and SARS-CoV-2.

SARS, the 21st Centuries first pandemic, was initially identified in China’s Guangdong province, in late 2002, by medical practitioners who became aware of “unusual” cases of pneumonia, but did not report it to the World Health Organization (WHO). In early 2003 an outbreak in Hanoi, Vietnam, involving a WHO officer that later died, was reported as a large outbreak on the March 10th.

A physician that travelled from the Guangdong province to Hong Kong while infected with SARS stayed at the Metropol Hotel, reportedly transmitting the virus around a dozen guests. Three returned to Singapore, two of whom then returned home to Canada, one to Vietnam, one to Ireland, and one to the United States. Thus SARS began its spread around much of the globe, but with most cases occurring in Asia.

SARS was described as both aggressive, and with high lethality, symptoms were typically reported within two to three days, and with limited reports of infections in the absence of symptoms. One must recall variances in test capacity in regards to total cases when comparing SARS and SARS-CoV-2. The recent pandemic has seen Covid-19 testing reach massive scales, with the United States alone, as of December 2nd, 2020, performing >196 million tests for Covid-19. (3)

In April 2003 the WHO suggested laboratory diagnostics tests, stating that;

“researchers in several countries are working towards developing fast and accurate laboratory diagnostic tests for the SARS coronavirus (SARS-CoV). However, until standardised reagents for virus and antibodies detection are available, and methods have been adequately field-tested, SARS diagnosis remains based on the clinical and epidemiological findings: acute febrile illness with respiratory symptoms not attributed to another cause and a history of exposure to a suspect or probable case of SARS or their respiratory secretions and other bodily fluids.” (4)

This means clinical symptoms such as respiratory distress were indicated as a need for further differential diagnosis. Thus samples from “suspected and probable SARS cases” were tested for SARS-CoV using the following methodology.

“Laboratory test result criteria for confirming or rejecting the diagnosis of SARS remain to be defined.

Molecular tests (PCR)
Polymerase chain reaction (PCR) can detect the genetic material of the SARS-CoV in various specimens (blood, stool, respiratory secretions or body tissues Sampling for Severe Acute Respiratory Syndrome (SARS) diagnostic tests). Primers, which are the key pieces for a PCR test, have been made publicly available by WHO network laboratories on the WHO web site. A ready-to-use PCR test kit containing primers and positive and negative control has been developed. Testing of the kit by network members is expected to quickly yield the data needed to assess the test’s performance, in comparison with primers developed by other WHO network laboratories and in correlation with clinical and epidemiological data.

Principally, existing PCR tests are very specific but lack sensitivity. This means that negative tests cannot rule out the presence of the SARS virus in patients. Furthermore, contamination of samples in laboratories in the absence of laboratory quality control can lead to false-positive results.
Positive PCR results, with the necessary quality control procedures in place. Recommendations for laboratories testing for SARS-coronavirus, are very specific and mean that there is genetic material (RNA) of the SARS-CoV in the sample. This does not mean that there is live virus present, or that it is present in quantity large enough to infect another person.

Negative PCR results do not exclude SARS. SARS-CoV PCR can be negative for the following reasons: - The patient is not infected with the SARS coronavirus; the illness is due to another infectious agent (virus, bacterium, fungus) or a non-infectious cause. - The test results are incorrect (“false-negative”). Current tests need to be further developed to improve sensitivity. - Specimens were not collected at a time when the virus or its genetic material was present. The virus and its genetic material may be present for a brief period only, depending on the type of specimen tested.

2. Antibody tests

These tests detect antibodies produced in response to the SARS coronavirus infection. Different types of antibodies (IgM and IgG) appear and change in level during the course of infection. They can be undetectable at the early stage of infection. IgG usually remains detectable after the resolution of the illness.

The following test formats are being developed, but are not commercially available yet: - ELISA (Enzyme Linked ImmunoSorbant Assay): a test detecting a mixture of IgM and IgG antibodies in the serum of SARS patients yields positive results reliably at around day 21 after the onset of illness. – IFA (Immunofluorescence Assay): a test detecting IgM antibodies in serum of SARS patients yields positive results after about day 10 of illness. This test format is also used to test for IgG. This is a reliable test requiring the use of fixed SARS virus on an immunofluorescence microscope.

Positive antibody test results indicate a previous infection with SARS-CoV. Seroconversion from negative to positive or a four-fold rise in antibody titre from acute to convalescent serum indicates recent infection.

Negative antibody test results: No detection of antibody after 21 days from onset of illness seems to indicate that no infection with SARS-CoV took place.

3. Cell culture

Virus in specimens (such as respiratory secretions, blood or stool) from SARS patients can also be detected by inoculating cell cultures and growing the virus. Once isolated, the virus must be identified as the SARS virus with further tests. Cell culture is a very demanding test, but currently (with the exception of animal trials) only means to show the existence of a live virus.

Positive cell culture results indicate the presence of live SARS-CoV in the sample tested.

Negative cell culture results do not exclude SARS (see negative PCR test result).” (4)

Case detection in 2003 SARS pandemic took a different approach to SARS-CoV-2 in 2020, and the closest similarities may be seen potentially at the early onset of what became Covid-19 before the mass rollout of tests occurred outside of laboratory settings.

In 2003 severe respiratory illness needed to be within the context of “documented exposure risk” when diagnosing SARS-CoV disease. SARS-CoV disease was thus to be investigated in patients hospitalised for:

“Radiographically confirmed pneumonia or acute respiratory distress syndrome of unknown aetiology, AND
One of the following risk factors in the ten days before illness onset:
Travel to mainland China, Hong Kong, or Taiwan, or close contact with an ill person with a history of recent travel to one of these areas, OR
Employment in an occupation associated with a risk for SARS-CoV exposure (e.g., healthcare worker with direct patient contact; worker in a laboratory that contains live SARS-CoV), OR
Part of a cluster of cases of atypical pneumonia without an alternative diagnosis” (5)

 Masks were used across parts of Asia, temperature scanners were introduced in major public gathering places, with quarantines implemented. A peak in viral infection seemed to occur around late May of 2003 before SARS-CoV seemingly disappeared the strict quarantine measures credited when the WHO declared the threat over.

Data on the number of tests carried out during the 2003 epidemic seems scant, no doubt diagnostic attempts were drastically ramped up for the 2019-2020 emergence of a “novel” coronavirus. I part that context needs including within the suggestion that 2003 SARS had a higher risk for mortality, but did not infect so many or last as long. One must consider that in 2020 after failure to implement testing, alongside track and trace (considering that the United Kingdom Government abandoned this strategy initially), testing was eventually conducted beyond the 2003 SARS criteria, including those that had little to no symptoms and or had been identified for testing by studies and contact tracers. As such, one may consider the sudden disappearance of SARS occurred due to searches being limited to those with more serious manifestations of SARS pathology. Hence the mortality rate was also substantially more severe in 2003-2004.

Concerning a SARS vaccine, the studies for SARS-CoV-1 were initiated and tested in began in animal models (this phase was bypassed in favour of human trials with the Covid-19 trials), with an inactivated whole virus being tested in mice, ferrets, and nonhuman primates. These studies  suggested the vaccine provided protective immunity, but sadly in the animal studies it seemed to cause immune disease, specifically an immunopathologic-type lung disease, which given the nature of SARS was not a good outcome. (6)

Human studies were not conducted, and the vaccine studies petered out due to the apparent disappearance of the virus, which was attributed to a number of factors, including the weather in the summer (a fear during the Covid-19 trials was that participants would not be sufficient as the disease prevalence lowered in the summer months), the “strict quarantine initiated of not only those infected but those who had been in contact with individuals sufficiently identified as infected. In reality, nobody knows why the pandemic ended; viruses tend to be unpredictable. However, as written by the author in Pandemic Panic (7), viruses tend to mutate to less severe strains to survive. A virus that is either lethal to all hosts, or renders hosts unable to circulate in the community leads to less spread, and the virus cannot survive. Potentially in SARS, the increased mortality rate may have caused such a phenomenon. However, it seems more plausible, given that while mortality was suggested to be higher than SARS-CoV-2, it did not kill all those infected, that limitation of testing to those formally diagnosed as being infected led to the less severe strains running unchecked in so-called asymptomatic individuals. In SARS-CoV-2, mild and asymptomatic cases are being highlighted, giving the impression that this latest pandemic is less lethal but more virulent. Vaccine development for SARS-CoV-2 varies, with some using minute viral portions, or virus ribonucleic acid (RNA). (8)

This is suggested to circumvent the issues that occurred with the SARS-CoV-1 vaccine that relied upon greater amounts of the actual virus.

BioNTech and Pfizer recently announced preliminary "evidence," and in the United Kingdom following hasty checks which some suggest to be a political move by a government reeling from the looming disasters of Brexit, and the poor handling of the pandemic. The United Kingdom became the first to approve the Pfizer/BioNTech vaccine, paving the way for so-called "mass" vaccination, after Britain's medicines regulator, the MHRA, suggested the product which allegedly offers "up to" 95 per cent "protection against Covid-19 illness," was safe enough to be rolled out. (9)

The news was greeted with much excitement, but one must consider that "up to" 95 per cent and "protection against Covid-19 illness" are not well defined.

The approval of an mRNA vaccine for use is a world first (10), and while the technology appeared in 1990 within the literature, it has been fraught with numerous issues that needed solving.

Vaccines in theory work via introducing material that is sufficient and specific enough to provoke an immune response. This is in theory achieved by an attenuated (weakened) virus, a virus that has killed, or a viral protein, such as occurs in an mRNA vaccine, in which a messenger RNA is introduced, this RNA is the genetic material utilised to translate the proteins used within our bodies.

The typical self/non-self model of immune function whilst still the predominant held view in immunology, and general practice has encountered problems since the 1980s. Dr Matzinger's Danger Theory (11), argues that tissues are a large factor in driving an immune response and that one occurs in response to a danger which may vary not only by the specific threat, but between individual response to a threat (e.g. older individuals may have a lower threshold). What may present danger to one, may not represent the same degree of risk to another. Certainly, this needs to be accounted for in vaccines that do not contain a live virus, and also in those with attenuated virus samples. Viruses that have been inactivated are less dangerous and produce a weaker immune response, necessitating immunologic adjuvants, and often multiple "booster" injections. (12)

Adjuvants in immunology refer to substances included to potentiate and improve the immune response. (13) Vaccine manufacture was assumed to cause significant variability in batch efficacy due to contamination within reaction vessels used within processing, however, when cleaning protocols were scrupulously increased, a reduction occurred in vaccine "effectiveness," and contaminants were noted to "enhance" the immune response. (14)

As can be seen at the beginning of the article, the vaccine includes the RNA ingredient BNT-162B2, and several other ingredients or adjuvants, namely;

lipid ALC-0159 (UNII: PJH39UMU6H)
lipid ALC-0315 (UNII: AVX8DX713V)
POTASSIUM CHLORIDE (UNII: 660YQ98I10)
MONOBASIC POTASSIUM PHOSPHATE (UNII: 4J9FJ0HL51)
SODIUM CHLORIDE (UNII: 451W47IQ8X)
SODIUM PHOSPHATE, DIBASIC, UNSPECIFIED FORM (UNII: GR686LBA74)
SUCROSE (UNII: C151H8M554)

Adaptive immune response theoretically occurs following an innate immune response (danger) that see cells such as the dendritic cells being engulfed by the pathogens, which migrate to lymph nodes and then causing reactivity in T cells that act as the adaptive immune cells. (15)

This activation causes mast cells to release both heparin and histamine that isolates the infection site to enable immune cells to clear out pathogens but also causes the release chemokines. Adjuvants are suggested to increase the local reactions and induce a larger release of danger signals, plus induce the release of inflammatory cytokines. The immune system is suggested to recognise these pathogenic molecules due in part to Toll-Like Receptors (TLRs).

Various medical complications are suggested to occur both in humans and animals due to adjuvants, with aluminium salts, utilised in numerous vaccines but regarded safe by the Food and Drugs Administration. (16)  Yet, numerous studies indicate a role in the development of Alzheimer's disease (17), in which adjuvants may be too reactogenic, creating susceptibility to fever. Indeed fever post-vaccination is an expected outcome. The vaccination for "swine flu" H1N1 pandemic was associated with the incidence of the chronic sleep disorder, narcolepsy in both children and adolescents (18), which associated with an influenza vaccine called Pandemrix that has the AS03-adjuvant.

In animals, specifically mice, aluminium adjuvants which have been previously linked to Gulf War syndrome (GWS), following its use in anthrax vaccination, has been indicated to cause motor neuron death (19), increases in incidences of amyotrophic lateral sclerosis, as well as other related neurological disorders correlated with GWS. No doubt multiple environmental variables are noted, anthrax vaccination and the relevant adjuvants such as aluminium hydroxide and squalene have repeatedly and increasingly faced scrutiny. The use of squalene, a suspension of oil-water is also indicated as increasing the risk for auto-immune disease incidence in rodents. (20) Squalene itself is indicated in arthritis prone rodents as inducing rheumatoid arthritis. (21) A 2006 report by Richards et al. (22), found a relationship between vaccine-associated sarcoma (VAS), but conflicts exist on whether specific vaccines increase risk, manufacturing processes specifically, adjuvants, or other associated variables. (23).

On the 8th December 2020, the United Kingdom began rolling out the Pfizer vaccine candidate, an mRNA (messenger RNA) type of vaccine as previously discussed, that enables synthetic genetic material which is enveloped in lipids to transfect (infect) the cell, which occurs due polyethylene glycol (PEG). In what is often referred to as conspiracy theory circles, public awareness usually focuses upon PEGs use in anti-freeze type products that may be utilised in motor vehicle radiators amongst other uses. PEG aids in the Nucleoside modified mRNA encoding for SARS-CoV-2 full-length spike protein antigen and is combined with a lipid nanoparticle (LNP) formulation. (24)

Polyethylene glycol forms part of the formulation of lipid nanoparticle that envelops the specific mRNA genetic material, which was previously noted as ALC-0159, which is the name for 2[(polyethylene glycol)-2000]-N,N-ditetradecylacetamide. (25)

Knop et al. (26), reviewed the use of polyethylene glycol in delivery of pharmaceutical drugs, indicating that as early as the 1950s they were linked to a propensity to cause cellular clumping and blood clotting, which increases the risk for embolisms, including pulmonary embolisms, as well as inducing an inflammatory cytokine storm. Polyethylene glycol is suggested to be linked to high incidences of drug-related adverse reactions, including but not limited to anaphylaxis. (27; 28; 29; 30; 31; 32; 33; 34; 35)

Indeed, as indicated by Pottel et al. (36), medications tend to constitute relatively minute amounts of the active pharmaceutical ingredient, with the majority of tablets, capsules, liquids, and injectables such as vaccines including numerous components such as dyes to help distinguish drugs, preservatives to ensure stability and shelf life. Alongside antimicrobials and excipients compounds that may be either act as fillers or as is suggested in vaccines, it must be essential to ensure the active ingredient is delivered "safely" and effectively (i.e. create immune response).

It is generally accepted that ingredients listed as excipients are biologically approved due to an absence of acute toxicity in studies using animals. Pottel et al. (36), searched for subtle long-term effects, and interaction with other medicines, stating that many excipient effects may have been previously unappreciated and may play an important role in health outcomes and disease.

The use of lipid nanoparticles in the Pfizer vaccine, like one from Moderna, is suggested to be approximately 100 nanometers in diameter, similar to the actual coronavirus. Pfizer suggests it uses four different lipids in a "defined ratio", with lipid ALC-0315 being a primary ingredient within the formulation that is ionisable and can be positively charged. At the same time, the RNA has a negative charge causing the two to attract each, but that it is a component known to able to cause side-effects. (37)

Errors made by the Scientific Advisory Group for Emergencies (SAGE), ones that have continued throughout the pandemic, were discussed in other works by the author (7), made the assessment of the unfolding SAR-CoV-2 pandemic predictions grossly inaccurate, which was seen to have both disastrous effects upon the nation's response to Covid-19, and also necessitated frequent and drastic re-evaluated estimates. SAGE's initial estimates followed a narrative that SARS-CoV-2 was a novel coronavirus and that the cases found in late 2019 were the initiation of its spread. Thus the pandemic was in early stages, and that the majority of the United Kingdom population (as high as >93 per cent) had not been exposed to the virus and were at risk of infection. A failure to act would lead to 500,000 deaths if no action were taken. (38)

This modelling assumed the total population to be susceptible to SARS-CoV-2, with no pre-existing degree of immunity present within communities. Yet as described by Doshi (39), who highlights six specific studies that report SARS-CoV-2 T cell reactivity in between 20 to 50 per cent of individuals with no documented viral exposure.

Ng et al. (40), studying samples of blood collected in the United States between 2015 and 2018, found 50 per cent had some form of SARS-CoV-2 T cell reactivity. Weiskopf et al., utilising specimens collected in the Netherlands found T cell reactivity in two out of 10 individuals that had not been virally exposed. (41)

Further reactivity was identified in individuals in the United Kingdom, Germany, Sweden, and Singapore. (42; 43; 44; 45)

Whilst small in scale and unable to provide accurate estimates of whom might have prior immunological SARS-CoV-2 responses, that findings indicated across continents, and various laboratories suggest that further research is warranted.

Chavarria-Miró et al. (46), indicate the detection of SARS-CoV-2 in sewage retrospectively tested in Barcelona, long before their first case of Covid-19 presented. This suggests that SARS-CoV-2 was present within the population prior to reports of a global pandemic.

Indeed, Basavaraju et al. (47), indicated SARS-CoV-2 infections within the United States in mid-December 2019, further evidence that supports the notion that this strain of coronavirus was spreading throughout many nations before the reports of initial cases in Wuhan, China. Sadly, entering further into such narrative potentially labels one as a "conspiracy theorist", a term some suggest is linked to the United States Central Intelligence Agency (C.I.A). (48) That said, failure to consider all theories and possibilities risks one being a "complicity theorist."

Anyone reading The Devil's Chessboard by Talbot (49), will have little doubt of the levels the United States have previously, and presumably will still go to maintain and further their cause. The book details the morally corrupt and somewhat cynical rise of the United States intelligence apparatus that documents from official records and their capability to intervene clandestinely in internal affairs of both competing nations and on a domestic front.

From the fanaticism brought on by the Cold War against Soviet Russia, and the "necessity" for unaccountable secret institutions to distort home politics and undermine the "democratic" elsewhere. One must draw parallels with the ideology to secretly fight communism, even to the degree that Dulles engaged in secret activities following World War Two, working to establish "ratlines" that aided Nazis considered useful to the United States in the new Cold War against the Soviet Union could both travel to the U.S, and avoid prosecution, and the secret testing on many U.S citizen via the MKULTRA project. (50) Dulles led the CIA-engineered coup in Iran in 1953 that toppled the democratically elected government of Mohammad Mossadegh and installed Shah Reza Pahlavi (who ruled until 1979) an apparent bold and daring triumph for the United States in the cold war against the Soviets.

In an era in which Wall Street is untouchable, China may be the United States current fear. Whilst stories should be considered and rationalised, it is not farfetched to suspect that we will read about these aspects at some point via declassified intelligence documents long in the future. The 6th August 2019 saw the United States main laboratory facility for biological warfare being issued a "cease and desist" order due to safety standards, protocol, and leaks violations. (51) Whether this was a convenient back story to cover for any clandestine activity remains unknown, but it all adds to the plausible deniability, a central tenet of CIA activity.

What do we know about the facility? Numerous experiments were engaged in by the United States. From the case in 1954, when seven inmates, notably all were black males, were isolated and fed mass doses of Lysergic acid diethylamide (LSD) for 77 days by Isbell. (52) "Work/research" that formed part of a highly secretive C.I.A program attempting to develop methods for mind control that was based at an inauspicious Army base, Fort Detrick.

Fort Detrick in Frederick, Maryland, just 50 miles from Washington was initially selected as a site for the development of secret plans for germ warfare. Until recently it thrived as the Army's principal biological research base with approximately 600 buildings spread across 13,000 acres. Through declassified documents that were not destroyed, we can establish that secret programs occurred to develop biological weapons, such as the Whitecoats. (53; 54; 55)

Little has been said regarding Covid-19 by Fort Detrick, and that little mention is made of Covid-19 seems curious given the study available freely on available (56), by Hensley et al.

Lisa E. Hensley is described as the Associate Director of Science at the Office of the Chief Scientist, National Institute of Allergy and Infectious Disease Integrated Research Facility in Frederick, Maryland. Before that acting as a civilian microbiologist in the virology division of the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) also located on Fort Detrick, Maryland. Acting as a subordinate lab to the U.S. Army Medical Research and Development Command (USAMRDC), which is also headquartered on the same installation. (57) Hensley is one of the premier researchers of some of the world's most dangerous infections, including Ebola hemorrhagic fever, and Severe acute respiratory syndrome (SARS). Holding various patents for vaccines and treatments, Hensley seems to be erroneously forgotten in the current climate. (58; 59; 60)

Is it likely that the intelligence services wished to impact China or its own citizens with a viral infection? Hopefully not, but given past actions, and the serious breaches in safety, one would expect a better account to explain such instances. The United States seems to be positioned as ever to maintain plausible deniability. Is it possible that SAR-CoV-2 was already present in the United States and other nations, and Wuhan, China was simply the site at which it was formally identified?

In the United Kingdom, and indeed many other nations, one must first consider that the scientific advisory group for emergencies (SAGE), consisted of no clinical immunologists, nobody with a degree in biology, or post-doctoral specialisations specifically in immunology. Some were medics, but sociologists, psychologists, economists, political theorists, and a profuse amount of mathematicians formed the modelling group responsible for much of the pandemic response. (61)

Modelling does require specific expertise to achieve their desired outcomes. Such outcomes may not specifically be based on the full available evidence, but in an ideological stance that misses context and skews the outcome predictions. When modelling is structured by those with little expertise in the specific subject-matter, it risks foundational errors that are missed by the modellers, and often by those tasked with implementing policy and operational changes due to a false belief in the disproportionate power of models. However credulous the modelling group within SAGE may appear, the claims made about the processes and pathways of pathological diseases such as Covid-19 fails to account for specific biological variables and makes assumptions of crucial factors such as the starting point for SARS-CoV-2 spread.

The models utilised on the suggestion of Imperial College were inherently flawed for several reasons. However, primarily as discussed above, that SARS-CoV-2 was a novel virus, and thus conferred no prior immunity within the community. As has been discussed earlier, the evidence currently suggests SAR-CoV-2 emerged before the date in contemporary literature and the media, and that T-cell reactivity is evident to some degree of the population, which would be expected given that SARS-CoV-2 is a mutation of the coronavirus and not a totally new emerging virus. (62)

This assumption that 100 per cent of the population were susceptible to SARS-CoV-2 infection led to a further false belief that studies of antibodies within the blood allowed a model to be constructed that determined the percentage within the population that had been infected.

SAGE suggested as of September 2020 that >90 per cent of the United Kingdom population remained at risk. (63) Which when combined with the “data” from the REal Time Assessment of Community Transmission (REACT) study suggests “that slightly under 6 per cent of the population may have antibodies for the virus by the end of June…” indicating that such individuals were “likely” to have been exposed to SARS-CoV-2, or suffered with Covid-19 “disease”. (64)

One could therefore assume that the United Kingdom government-backed stance on SARS-CoV-2/Covid-19 risk suggest that circa 94 per cent of the population have not been infected. A figure which seems disconcertingly high when one considers the narrative that while SARS-CoV-2 carries less mortality risk than SARS, it is suggested to be more prevalent and spread more easily, even within individuals classified as asymptomatic, i.e. people who are not displaying symptoms of the disease.

The official data suggests a fatality rate circa 3.5 per cent (65), with 1,766,819 positive tests, and 62,566 deaths recorded “with” Covid-19 identified. With a U.K. Population of 68,045,779, a six per cent infection rate should mean that over four million eighty-two thousand seven hundred forty-six people have been, or are infected, which gives a fatality rate of approximately 1.5 per cent.

However, as discussed, it seems curious that SARS-CoV-2 would infect such a low population percentage, even if one considers that it only began its global spread in December 2019. Indeed, Ioannidis (66) studied globally collated data suggest an infection fatality rate circa 0.2 per cent as the best estimate.

This error or flaw in the policies and models comes from the initial assumptions that SARS-CoV-2 was a novel virus. While the event that led to finding SARS-CoV-2 made it seem novel, we neither know how long it existed undetected nor know the immunity granted from prior coronaviruses infections. In short, viruses have genetic ancestors, and the previous “novel” coronaviruses already discussed, 2003 SARS and 2012’s MERS in 2012 (67), have similar DNA sequences and structures to the current virus, with SARS being indicated to be as much as >85 per cent identical.

In prior work (7), I spoke about endemic coronavirus that remain linked to the common cold, which continues to circulate freely within both within the United Kingdom and globally. Modernity, specifically a tendency to remove sick pay in less affluent social communities, seems to cause a faster and easier transmission of such viruses. Human coronaviruses (hCov), such as hCoV-HKU1, hCoV-OC43, hCoV-NL63 and hCoV-229E are discussed in detail by Zhu et al. (67) While discovered in the 1920s in animals (68; 69), it wasn’t until the 1960s that human coronaviruses were identified. (70; 71; 72; 73; 74) As before, discovery does not mean they were non-existent and newly emerged, just that research has “isolated” and identified something which was considered new. That hCoV-HKU1, hCoV-OC43, hCoV-NL63 and hCoV-229E tend to either led to asymptomatic or mild type respiratory and/or gastrointestinal infections, does not discount from their circulation within humans since their first identification, and no doubt before their documented existence. While accounting for between five to 30 per cent of all common colds, hCoVs are rarely considered serious until the occurrence of global pandemics such as in SARS-CoV, MERS-CoV and SARS-CoV-2.

Initial opinions of coronavirus appear to have considered them to be relatively harmless pathogens, yet they have become globally associated with potential severe clinical complications in recent months. Coronavirus, an enveloped type virus identified by a positive-strand ribonucleic acid (RNA) genome, primarily targets mucosal surfaces within both respiratory and the intestinal tracts in various mammals and birds. (75; 76)

Human coronavirus isolates known as hCoV-229E and hCoV-OC43 were correlated with the “common cold”, and symptoms in the upper respiratory tract that are both mild and self-limiting. (77; 78) When the so-called new variant SARS-CoV was discovered, which initiated an outbreak globally of acute instances of often severe cases of atypical pneumonia, circa 2003, led to an interest in human coronaviruses and the identification of two further novel variants, HCoV-NL63 and HCoV-HKU1. (79; 80) These showed an ability to cause serious complications in the respiratory tract, particularly in patients with existing comorbidities.

The initial discovery of human coronaviruses in the 1960s (70; 81), involved two different isolation methods. One, by Kendall, Byone and Tyrell (82), at the British Medical Research Councils Common Cold Unit, in which B814 a common cold novel virus that was unable to be cultivated using standard techniques previously used to successfully cultivate adenoviruses, rhinoviruses, and others associated with the common cold. (83) Tyrell and Byone instead used a method in 1965, that involved serial passage through a human embryonic trachea organ culture. A 1966 paper by Hamre and Procknow (84), from the University of Chicago, describes the isolation of another novel cold virus, hCoV-229E, which was sourced from medical students, and grown in a culture of kidney tissue.

Human coronaviruses are indicated to act with renin-angiotensin proteases (enzymes that breakdown proteins and peptides). To both establish and maintain a cycle of infection, coronaviruses require that they deliver genetic material inside the intracellular space, mediated by glycosylated spike proteins, which are discussed in other works. (7)

Angiotensin Converting Enzyme 2 (ACE2) is suggested to act as a functional receptor for human coronaviruses (9), with antibodies that direct against ACE2 theorised to prevent SARS-CoV infection. (85)

The renin-angiotensin system (RAS), is a well-described endocrine system, vital in the maintenance of cardiac function, arterial pressure, homeostasis of fluid, and salt balance, along with regulation of tissue remodelling, particularly in the proliferation of cells, angiogenesis and apoptosis. (86)

Aside to the physiologically normal processes, RAS is correlated with a variety of pathophysiological actions. (87) Abnormal RAS activation is established as a variable in the development of numerous cardiovascular diseases, including hypertension, diabetes and renal disease. (88; 89)

Within RAS, synthesis of a variety of angiotensin peptides occurs, which are degraded by the precursor angiotensinogen via a series of complex enzymatic reactions. Specific components of RAS generate within specific body regions. For example, renin is generated within the kidneys, while ACE is derived from the lungs, with the liver responsible for angiotensinogen. Angiotensin synthesis is suggested to be evident to some degree in all organs, RAS activity initiates via the kidney, following juxtaglomerular cells releasing renin (90; 91), which acting as an aspartic protease works to cleaves its substrate angiotensinogen, that is then produced in the liver and forms the inactive angiotensin peptide, Ang I or Ang 1–10. Ang I converts to either And II, a RAS effector peptide, or Ang 1–8 via the protease ACE which is dependent on zinc. (92)

Higher ACE expression occurs on vascular endothelial cell surfaces, in particular within lung tissue. (93) Ang II generation from Ang I can occur via enzymes that are not ACE related, such as chymase, a serine protease. Whilst ACE is considered to be the primary enzyme responsible for Ang II-conversion, research indicates that Ang II conversion occurs via chymase enzyme in certain pathological vascular conditions. Indeed, it must be noted that chymase activity is evident in pulmonary membranes, aiding Ang I conversion into Ang II within lung tissues. (94)

RAS is typically considered a system of endocrine and circulation predominantly. Yet, it is now well established that alongside RAS peripherals, RAS is both tissue-specific and abundant in independent localised systems. Indeed, within various organ systems, such as the lungs, kidneys, liver, heart, brain, vasculature, pancreas, and within the reproductive, nervous, and the digestive system. (92)

In-spite speculation regarding the existence of RAG local airway capacity intrapulmonary generation of Ang II was a recent confirmation. (95)

Alveolar mast cells within both the lower and upper respiratory tract are evidenced to express renin levels, which triggers the formation of pulmonary Ang II. (96;97)

RAS components are also abundant in airway tissue in humans, including ACE and angiotensinogen, with pulmonary epithelium evidenced as the primary circulatory source for ACE. (98)

Receptors for Ang II are evidenced to be expressed within lungs, in the form of the subtype AT1 which is found in the smooth muscle bronchial cells, and bronchial receptors AT2 receptors within the epithelial brush borders. (99)

The expression of ACE2 in both alveolar, bronchiolar epithelial cells, and pulmonary endothelial cells is well documented. (100)

Lung masts cells are evidenced to have chymase, potentially being the major enzyme responsible for Ang II-generation within the lung. Local RAS activity within pulmonary tissue has been indicated as contributory in tissue remodellings, such as alveolar epithelial cell apoptosis regulation, fibroblast proliferation, and collagen production within the lung. (101; 102)

Thus, it is suggested that activation that is inappropriate with regard to specific local components of the airway RAS, specifically ACE2, may initiate factors that exacerbate the pathophysiological development of symptoms associated with SAR-CoV-2, and the severity of disease outcome in covid-19.

ACE2 and SARS-CoV-2

Angiotensin-converting enzyme 2 (ACE2), plays a major role in RAS homeostasis, converting Ang II to Ang (1–7), and the activation of the RAS putative pathway. ACE2 is thought to be responsible for regulating net Ang II tissue levels, as an antagoniser of fibrotic and hypertrophic effects due to the AT1 receptor being the binding site of Ang II. (103; 104)

ACE2 may exhibit a role of counter-regulation that seems critical for RAS homeostasis within the lung. (104; 105) Thus, improper regulation leads to increases in both ACE and Ang II levels which are associated with the pathogenesis of numerous variations of lung disease, such as sarcoidosis, pulmonary hypertension, pulmonary fibrosis, and more importantly in the context of COVID-19, acute respiratory stress syndrome (ARDS). (106; 107; 108)

Studies conducted in-vivo confirm an association between the severity of ARDS, and the outcome, with pulmonary RAS. (109) ARDS, a severe acute lung injury, is characterised by an accumulation of inflammatory cells, pulmonary oedema, and severe hypoxia (110), as prevalent in documented cases of covid-19. ARDS may be triggered by various pathogenic states, such as sepsis, pancreatitis and severe trauma/shock. (111)

Previous studies indicate pulmonary RAS in ARDS pathogenesis, and that ACE antagonists such as AT1 receptor blockers delay the onset of ARDS in rodents exhibiting acute lung injury. (112)

Negative contributions of ACE to the pathogenesis of ARDS occurs via a variety of mechanisms, such as increases in vascular permeability. (113)

Imai et al. (109), identified a protective role of ACE2 during acute lung injury such as ARDS, in counterbalancing the induced pathophysiological effects of angiotensin II. Mice bred with an abrogated expression of ACE2 expression exhibited more severe disease patterns than control mice, with an enhanced degree of vascular permeability, lung oedema, and decreased lung function.

SARS-CoV & HCoV-NL63 in relation to RAS activity

The 2003 epidemic of SARS-CoV, was a disease that remained relatively rare, with an incidence 8,422 cases, and a total fatality rate of circa 11 per cent (114), which is primarily suggested to be attributable to ARDS induced respiratory failure. Indeed, the fatality rate is variable, mostly dependent on factors such as age, and treatment methodology, to be between 0 and 50 per cent (115), with SARS patients < 24 years evidenced to be less likely (< one per cent) to die from SARS, that those > 65 who had a 55 per cent mortality rate. (116)

SARS-COV infects host cells via ACE2, the component of RAS, which is evidenced to protect against ARDS induced acute lung failure. (117; 118)

As aforementioned, the spike protein engages with ACE2, and a reduction occurs in the cell surface. Thus ACE2 functional capacity is down-regulated (117; 119), a phenomenon that is evidenced to provoke increased severity and risk of lung failure in rodents infected it SARS-CoV. (120)

It is also worthy of note that the within the SARS-CoV-2 spike protein, a pocket of the free fatty acid, linoleic acid has been indicated to increase SARS-CoV-2 binding (121),

Interestingly, despite this research, the team consider linoleic acid to be a viable potential therapy due to the fatty acids so-called "essential" nature.

Ling et al. (122), studied rodent fatty acid profiles alongside inflammatory markers utilising animals fed a diet considered essential fatty acid-deficient (EFAD) constituting 2 per cent hydrogenated coconut oil (HCO) for two weeks. Alongside groups supplemented with 1.3mg of arachidonic acid and 3.3 mg of docosahexaenoic acid (AA + DHA) which created a 2 per cent fat diet. Upon exposure to lipopolysaccharide, the rodents on the EFAD diet had significantly lower levels of various inflammation markers, such as tumour necrosis factor (TNF) and interleukin-6.

Increases in serum levels of C18 unsaturated free fatty acids are discussed by Bursten et al. (123), as being a significant predictor in acute respiratory distress syndrome (ARDS) development, which was examined within both Controlling Intuitive Appetite (124), and Pandemic Panic (7), which suggests that increases in ratios of unsaturated serum acyl chain occur between those codified as healthy and those patients which suffered severe outcomes, were both sufficient to identify those likely to suffer ARDS and provide insights regarding the essentiality of unsaturated fatty acids.

Hanna and Hafez (125), discuss arachidonic acid being an unsaturated fatty acid that is sourced either via direct dietary means or indirectly via the metabolism of linoleic acid. Its release occurs via the breakdown of phospholipids under the action phospholipase A2. Various factors, including mechanical through to chemical stimuli, may induce a cascade of arachidonic acid.

Malcolm et al. (126), compared the composition of fatty acid in adipose tissue samples taken from 143 adults autopsied humans aged 24 to 61 years, one from a deep-seated site (perirenal) two from subcutaneous sites, the buttock and abdominal areas. Proportional saturated fatty acid levels were highest in samples of adipose tissue found in the perirenal, whilst the adipose tissue buttock was lowest in saturated fatty acids. Proportionally level of both linoleic and linolenic acids was similar across all sample sites, leading them to conclude adipose tissue found in the buttock has a greater degree of unsaturation than abdominal adipose tissue.

Mamalakis et al. (127), in a study of 475 adolescents aged 11 to 18 years (138 aged 11 to 16 years completed all variables), assessed levels of physical activity, serum lipids, and both buttock and abdominal composition of adipose fatty acids, finding that like adults, the composition of fatty acid in the abdominal adipose tissue of children is supposedly less favourable that the buttock. With abdominal adiposity once again exhibiting the much-maligned elevated proportions of saturated fatty acids, with decreased proportions of both monounsaturated and polyunsaturated fatty acids when compared to buttock adiposity. Such findings are corroborated in adults by Pittet et al. (128), and Phinney et al. (129)


That unsaturated fatty acids are suggested as being important in the binding of the SARS-CoV-2 spike protein, and are indicated to be higher with age seems to correlate well with the susceptibility of aged subjects to SARS-CoV-2 infection and increased mortality.

The team (123) states that activity in the linoleic acid metabolic pathway can trigger both systemic inflammation, acute respiratory distress syndrome, and cause pneumonia, all pathologies observed in severe Covid-19, ARDS, Sepsis patients. (7)  

El-Kurdi et al. (130), concurs that mortality increases in relation to unsaturated fatty acid, both with exogenous consumption and administration and also due to adipose lipolysis. Indeed, as Covid-19 pathology worsens, dietary intake may reduce due to loss of appetite, which increases fatty acid oxidation, potentially of unsaturated fatty acid. Unsaturated fatty acids seem critical in the SARS-CoV-2 spike proteins' ability to attach and enter the human body, specifically via the ACE2 receptor.

Validation by research from Bristol University (121), which seeks a possible basis for a pharmaceutical intervention that may prevent the Sars-CoV-2 virus from entering the human body, consists of a research team, led by both Christiane Schaffitzel and Imre Berger. They that found unexpectedly that linoleic acid was exhibited within a pocket of the protein. Linoleic acid, a constituent of widely available linseed oil, is also a component of many industrial processes such as the manufacture of linoleum, a floor covering consisting of canvas with a preparation of linseed oil as a backing. Linoleic acid (18:2ω6; cis, cis-9,12-octadecadienoic acid) is the most highly consumed n-6 polyunsaturated fatty acid (PUFA) in the human diet (131) and can be obtained from vegetable oils such as sunflower, safflower, soybean, corn, and canola oils as well as nuts and seeds.

The maintenance of n-6 polyunsaturated fatty acids as a so-called "essential fatty acid" as they cannot be manufactured endogenously (132), which is suggested to be required, among other things, to maintain cell membranes in the lungs, which continues to be the consensus belief (133), despite issues with membrane theory as described by Ling (134), in which he discusses a;

"concept that the basic unit of all life, the cell, is a membrane-enclosed soup of (free) water, (free) K+ (and native) proteins is called the membrane theory. A careful examination of records shows that this theory has no author in the true sense of the word. Rather, it grew mostly out of some mistaken ideas made by Theodor Schwann in his Cell Theory. (This is not to deny that there is a membrane theory with an authentic author, but this authored membrane theory came later and is much more narrowly focussed and accordingly, can at best be regarded as an offshoot of the broader and older membrane theory without an author.) However, there is no ambiguity on the demise of the membrane theory, which occurred more than 60 years ago, when a flood of converging evidence showed that the asymmetrical distribution of potassium (K+) and sodium (Na+), observed in virtually all living cells is not the result of the presence of a membrane barrier that permits some solutes like water and K+ to move in and out of the cell while barring--absolutely and permanently -- the passage of other solutes like Na+. To keep the membrane theory afloat, submicroscopic pumps were installed across the cell membrane to maintain, for example, the level of Na+ in the cell low and the level of K+ high by the ceaseless pumping activities at the expense of metabolic energy. Forty-five year ago this version of the membrane theory was also experimentally disproved. Despite all these overwhelming evidence against the membrane-pump theory, it is still taught as verified truth in all high-school and biology textbooks known to us today. Meanwhile, almost unnoticed, a new unifying theory of the living cell called the association-induction hypothesis came into being some 40 years ago. Also little noticed was the fact that it has received extensive confirmation worldwide, and has shown an ability to provide self-consistent interpretations of most if not all known experimental observations that are contradicting the membrane-pump theory as well as other observations that seem to support the membrane pump theory."

and that it appears to be the molecule to which Sars-CoV-2 attaches itself to enter the human body, the persistent narrative of it as essential leads the researchers to conclude not that n-6 polyunsaturated fatty acids should be limited, both via consumption and lipolysis, but that their challenge is the development of a pharmaceutical drug which can distort the spike protein of Sars-CoV-2, thus preventing it attaching to the linoleic acid, pointing to similar drugs that have already been developed to avoid rhinovirus attaching themselves to the lungs. (135)

The study authors note that despite colossal investment searching for elusive human immunodeficiency viruses (HIV) vaccines, the medical community relied upon therapeutic anti-viral medications of varying efficacy to decrease disease mortality risk.

Dr Ray Peat (136), in an article titled "fats, functions & malfunctions", discusses both linoleic acid and arachidonic acid, as not only increasing lipid membrane permeability but that the whole cell increases in permeability. This causes structural proteins to bind throughout the cell, which is exhibited in fibrosis seen in both Covid-19/ARDS and septic shock, along with an increased affinity to retain water. This leads to generalised cellular swelling and localised swelling in the mitochondria that reduce oxidative function, and allows increased cellular calcium that activates cellular excitation and initiates a redox shift toward inflammatory states that ultimately leads to inappropriate growth and mass, as seen in fibrosis and cancer, or cell death.

Dr Peat highlights the impact of such cellular environments, and the effects of glycogen restriction, which may occur via increased energy demand, or energy restriction, either intentionally or due to metabolic dysfunction—stating that decreased glycogen stores lead to increases in the secretion of adrenaline that may act to liberate fatty acids from adipose stores. Following chronic dietary consumption of n-6 polyunsaturated fatty acids, the ability to be oxidised or detoxified by the liver is impacted by glycogen availability and thyroid function. (137)

Peat (136), draws awareness to research by Cook et al. (138), Li et al. (139), and Autore et al. (140), and the quite remarkable resistance displayed by animals deficient in so-called “essential fatty acids to shock. This indicates the central role of polyunsaturated fatty acids in the maladaptive, and often chronic adaptions caused by acute shock, such as retention of calcium, cellular leakiness, and energy production inhibition, which bear striking similarities to the markers of many disease pathologies, and so-called “normal” ageing. The abundance of serum free fatty acids and stress hormones that tend in aged subjects to be both chronically higher, and result in poorer outcomes in diseases such as Covid-19 and other respiratory illnesses, alongside reduced tolerance of incidences of stress.

Much research indicates that animals with lower levels of unsaturated fatty acids exhibit higher metabolic rates, and a preference for glucose utilisation, which leads to increased carbon dioxide production (141), and enhanced resistance to toxins such as cobra venom (142), and lipopolysaccharides, commonly known as endotoxins. (139) This correlates with the discussion in Consistent Eating (143), that metabolism decreases in line with energy intake through the lifespan. That susceptibility to stress decreases as metabolism declines, suggesting a lower respiratory quotient due to limited glucose intake and increased consumption of fatty acids and protein.

Despite the associations with ACE2, identified polymorphisms in human ACE2 genes are not correlated with SAR-CoV disease progression. (144; 145)

Functional performance of RAS is evidenced to decrease as part of “normal” physiological processes of ageing, as is exemplified by a progressive inhibition of circulating levels of renin and the plasma activity. (146; 147)

Indeed, ageing is a frequently noted variable in infections related to both SARS-CoV, and SARS-CoV-2 as a significant predictor of poor outcome. (148)

Thus, RAS function in elderly, and groups with co-morbid conditions may lead to worse outcomes regarding ARDS and acute injury due to an overall impairment in RAS activity.

That coronavirus activates inflammatory systems, particularly RAS, and with available medications to act as both angiotensin receptor blockers and inhibit ACE. Angiotensin converting enzyme enables the production of inflammatory proteins which increase blood pressure, and the correlation between angiotensin and serotonin is well established in regards to age-related inflammation. As lifespan increases, exposure to and production of angiotensin occurs, increasing blood vessel contraction, which creates greater clotting risk and increases fatigue, alongside inhibiting energy production. (149; 150)

The class one viral fusion spike protein, which while unique to coronaviruses, is a feature that mediates attachment to the host receptor in all species of CoV. (151) The N-glycosylated spike protein varies abundantly between the CoV species with lengths between 1100 to 1600 residues, and an estimation of molecular mass ranging to <220 kDa. The spike protein features trimers that form the spikes evident on the surface of the CoV particle, which may be between 18–23-nm, a factor which may cause issues in the reliance on reverse transcriptase-polymerase chain reaction (RT-PCR) testing. (152; 153; 154)

Reverse transcription-polymerase chain reaction (RT-PCR) is an established laboratory technique used to identify specific genetic materials present in a sample via a biochemical amplification process. The test has been lauded as a scientific advance of great importance to the field of molecular biology, with the foundation of PCR revolutionising DNA study and gaining its creator, Kary B. Mullis, the 1993 Nobel Prize for Chemistry. It uses primers to sequences the encoding and may involve a cross-reaction with the spike protein that detects SARS-CoV-2 and other hCoV during the sample collection (155), as well as other respiratory viruses. As discussed, some degree of immunity is conferred by previous exposure to similar viruses. (156)

Reported variances in illnesses range from mild symptoms to severe, and well-documented occurrences of death since SARS-CoV-2 was first confirmed and reported in humans.

The Centre for Disease Control (CDC) initially suggested the following symptoms “may” appear 2-14 days after exposure.

Fever
Cough
Shortness of breath (156)

Covid-19 was described as having a mortality rate of 2-3.48 per cent, depending on the source (157), which may be a statistical distortion due to issues with test validity, continuity and availability, as well as a lack of diagnostic testing in those that are suggested to be infected but asymptomatic and therefore do not report for testing. As is the case in any well documented global pandemic, patients that become critical standout, and with no clear evidence on actual rates of those infected, or the actual rate of mortality in the population.

Variances and confusion seem evident in the testing protocol, with many citing initial failures in test validity (158; 159; 160; 161), with nucleic acid tests (NATs) that are widely utilised for diagnosis of new cases being suggested to increase the likelihood that many such infections may remain undocumented. Presumably where false negatives are a possibility, so to must be false positives. Whilst relatively cheap, and potentially abundant, the use of NATs as one of the two primary methods for confirming Covid-19 presence in humans subjects involves collecting patient samples that are then tested for specific molecules relevant to the Covid-19 genetic material.

Under previous criteria, a diagnosis of Covid-19 needed to be confirmed by lab tests, specifically a nucleic acid test performed on swabs from a patient’s respiratory tract or blood. Yet issues exist in nucleic acid testing, with “false negatives” created by tests that are not sensitive enough requiring greater amplification (cycle threshold), problems in transporting and handling samples, and questions over the quality of sample collection. (162)

A nucleic acid test (NAT) is a procedure for the detection of a specific nucleic acid sequence to detect virus or bacteria via the genetic materials RNA (ribonucleic acid)/DNA (deoxyribonucleic acid), as opposed to antigens/antibodies. As the amounts of genetic material are typically small, techniques are used to amplify genetic materials, namely nucleic acid amplification tests (NAATs), such as a strand displacement assay (SDA), or transcription-mediated assay (TMA), as seems to be utilised in the specific Covid-19 polymerase chain reaction (PCR) test.

PCR typically involves a process of 20–40 repeated cycles of thermal temperature variation. (163)
Initialisation: Consisting of heating to between 94–96 °C (201–205 °F), or 98 °C (208 °F) for 1–10 minutes.
Denaturation: Heating to 94–98 °C (201–208 °F) for 20–30 seconds.
Annealing: Lowered temperature to 50–65 °C (122–149 °F) for 20–40 seconds.
Extension/elongation: The temperature typically raised to approximately 75–80 °C (167–176 °F), but can be as low as 72 °C (162 °F) 

This represents a single cycle, which is repeated to amplify the DNA

Final elongation: May be performed between 70–74 °C (158–165 °F) for 5–15 minutes.
Final hold: Cools to 4–15 °C (39–59 °F) for indefinite periods, including short-term storage.

Which brings about doubts in procedural effects, and assumptions made from studies involving the use of once-living intact organisms that are highly treated, potentially rendering data meaningless, and potentially creating conflict due to entropic changes. (164)

That the medical community has rallied to develop reliable molecular diagnostic tests has been aided by numerous research groups working to identify and sequence the viral genomes via open databases. As infections are suggested to increase, authorities sought methods to diagnose and reliable document cases accurately. Clinically, access to robust, and accurate data was dependent upon the isolation and cultivation of coronavirus from the broncho-alveolar lavage fluid via three patients classified as a probable outbreak source.

Electron microscopy, a technique fraught with issues previously discussed by Hillman (164), allowed observations of "typical" coronavirus morphology, whilst more classic use of light microscopy demonstrated a cytopathic effect upon epithelial cells in the human airway. From this, various international groups worked utilising this sequence data to produce primers for PCR tests that would support public health laboratories in the absence of an available commercial Covid-19 test.

The lab of Christian Drosten, of the Institute of Virology, Charité University Hospital, Berlin, and academic collaborators in Europe and Hong Kong (165), verified and assessed the test validity in the absence of both isolates of SARS-CoV-2 or indeed patient samples. Upon this basis, 250,000 kits, were dispatched by the World Health Organization (WHO), to 159 laboratories globally.

A Hong Kong University group developed two quantitative RT reverse transcription PCR tests (166), that target viral genome sequences deposited with GenBank, then validated against two clinical specimens via SARS-CoV-2/Covid-19 infected patients.

The RT-PCR test is suggested to be highly sensitive if used correctly, but notably when the cycle threshold (amplification) is increased. This produces significant problems in high-pressure settings. It remains unclear on the optimal type of clinical specimen, suggesting that the nasopharyngeal swabs give greater consistency than sputum samples. (167) Questions are also raised concerning consistency in cycle threshold between test (with variances in assays), and the cut-off point at which cycle threshold becomes too sensitive and detects dead viral fragments from previous infections. 

These early lab tests are suggested to "buy-time,' and give public health authorities some diagnostic tools before commercial products and kits become available at scale. In China, genome sequencing firm BGI Group of Shenzhen had distributed over 50,000 test kits across China by the end of January. On the 5th February, it opened an emergency test laboratory in Wuhan that processed 10,000 samples per day. Other companies developed their tests more slowly. 

Not all were relying on primer designs and protocols specified by academic laboratories or public health authorities. Rather than develop bespoke PCR tests, IDbyDNA was one of a handful of companies employing metagenomic nucleic acid analysis as a routine diagnostic and surveillance tool. Its existing Explify Respiratory test was a laboratory-developed test, able to identify over 900 respiratory pathogens, including viruses, bacteria, fungi and parasites, by comparing unbiased metagenomic data obtained from patient samples with a large repository of sequence data. 

It was suggested that it could already detect the SARS-CoV-2 strain. 

"We have now updated our data with the new coronavirus and are in the process of revalidating," 

Said co-founder and chief medical officer Robert Schlaberg. 

"The modifications are all on the data analysis side." 

That was, he stated, a more straightforward process than updating the physical assay. The actual data analysis took less than an hour, giving a total turnaround time from receipt of sample to test result of 36 hours. Although more expensive than PCR testing, the falling costs of sequencing could help to democratise this approach. The company is selling the technology as well as its testing services.

The suggestion that NAT tests falsely produce negative results in patients with the infection is complicated by suggestions that Computerised Tomography scans are able to clearly identify signs of viral infection, even though radiation creates tissue disturbances. (168)

The enactment of emergency measures created a situation in which large biotech and medical testing laboratories can develop and validate their tests. Yet, various sources are compiled to generate the data which becomes publicly available. Interestingly, despite the seeming fragility to the stock market, certain biotech companies' value seems to be increasing. (169)

As described above regarding testing, these probabilistic inferences rely upon clusters of so-called empirical evidence, which can be seen to lack validity. As discussed in Mandel (170), a problem discussed by Eddy (171), explains that the following problem is encountered concerning the accuracy of a medical test in aiding probability assessment;

"The probability of breast cancer is one per cent for a woman at age 40 who participates in routine screening. If a woman has breast cancer, the probability is 80 per cent that she will get a positive mammography. If a woman does not have breast cancer, the probability is 9.6 per cent that she will also get a positive mammography. A woman in this age group had a positive mammography in a routine screening. What is the probability that she has breast cancer? __ per cent."

which is shown by Casscells, Schoenberger, and Graboys (172), amongst others, that physicians frequently incorrectly interpret the actual probability. Using bayesian reasoning, as discussed by Mandel (170), physicians fare better when all the information is considered rationally. The proportion of patients in the scenario initially suggested to have breast cancer would be referred to as the prior probability. The possibility that those with breast cancer receive a positive mammogram and a positive mammogram will be received by an individual who has not got breast cancer are both known as conditional probabilities. This information would collectively be referred to as priors. Through its use, we could estimate the likelihood of breast cancer.

If a sample of 10,000 female participants is utilised, and 100 of those have breast cancer, of which just 80 have received a positive mammogram. Nine thousand nine hundred do not have breast cancer, yet 950 of them will also receive a positive mammogram. From this data, we can assess that 1,030 females out of the original 10,000 participants received a positive mammogram, yet only 80 will have cancer, just 7.8 per cent of the total group.

This gives us four groups:

80 females have both breast cancer and a mammogram that is positive. 
20 females that have breast cancer mammogram that is negative. 
950 females that do not have breast cancer but have a mammogram that is positive.
8,950 females that do not have breast cancer and also have a mammogram that is negative.

Most physicians, and indeed most people make a common error and ignore both the fractions of females with breast cancer and those without breast cancer that have a false-positive diagnosis. Instead, it focuses only upon those with breast cancer and a positive mammogram, commonly assuming that breast cancer's probability must be 80 per cent due to the positive mammogram evidence. Reliance upon one single data point ignores three available pieces of data, and relies upon the prior probability, disregarding the available conditional probabilities. If one utilises all known data or even searches for further data to estimate the probability, then we can revise knowledge.

Priors may be true. They may indeed reflect the reality, but without effective judgement against all available data, or if priors are held as defined and facts that are unchallengeable, beliefs may be given unsubstantiated credibility.

This highlights that Covid-19 testing accuracy is not known, that multiple variants of tests may have been utilised globally, nationally, and indeed across state-lines. Indeed, all diagnoses may not be via tests, with less severe cases that are self-isolated and reported as Covid-19. That said, so-called asymptomatic carriers of the infection may remain undiagnosed. Thus suggestions regarding mortality/fatality rates remain questionable.

We can draw out some data that helps from the cases in Wuhan, China. In Zhang et al. (173), we see that from a total of 140 cases, other comorbidity's were present, indeed from all instances the most prevalent underlying health issue was hypertension.

64.3 per cent of those in the Zhang et al. research had underlying health conditions representing 90 people.

Of those 90;
 
42 (30%) suffered hypertension
17 (12.1%) suffered diabetes
8 (5.7%) suffered fatty liver disease
7 (5%) chronic gastritis
7 (5%) coronary heart disease 
5 (3.6%) thyroid disease

We can even delve into the severity of these conditions and get the nuanced data,
In non-severe cases 82 cases were split by;
 
20 (24.4% ) hypertension
9 (11%) diabetes
4 (5%) fatty liver diesese
5 (6.1%) chronic gastritis 
3 (3.7%) coronary heart disease 
1 (1.2%) thyroid disease

And in severe cases (58 people);
 
22 (37.9%) hypertension
8 (13.8%) diabetes
4 (6.9%) fatty liver disease
2 (3.4%) chronic gastritis
4 (6.9%) coronary heart disease
4 (6.9%) thyroid disease

Giving  p-values of 

Hypertension - 0.85
Diabetes - 0.615
Fatty liver disease - 0.718 
Chronic gastritis - 0.700
Coronary heart disease - 0.448
Thyroid disease - 1.60

A p-value less than 0.05 (typically ≤ 0.05) is statistically significant. However, I often take odds with p-values (124) for data skewing, p hacking et cetera, and I would also be curious about the incidence of thyroid disease due to poor diagnostic terms within orthodox medicine.

The endemic spread of hCoV’s that produce the so-called common-cold enables some degree of immunity, not only to those specific viruses but also to those closely related, with SARS-CoV-2 being one such virus. The evidence that SARS and SARS-CoV-2 are approximately 80 to 85 per cent identical at the genome sequence (67) should indicate that some degree of immunity cross-over could be expected to be demonstrated in contamination of results indicating SARS-CoV-2 infection being due to other hCoV types.

A systematic review by Jefferson et al. (174) suggests that the RT-PCR test is so sensitive that it is susceptible to picking up other hCoV contaminants and that it potentially detects post-infection fragments of SARS-CoV-2 (or other hCoV) that are no longer live. According to the team, this may lead to over-diagnosis of Covid-19 that has occurred, specifically in the so-called second wave of the pandemic.

One of the authors of the study, Professor Heneghan suggests that the findings should be used to classify whether test outcomes that are currently "positive or negative" depending on detection of "the virus", could be refined with a viral cut-off point. In which viral amounts are considered regarding how much trigger what would classically be called a case, indicated by symptoms and illness, not the current definition of a case which is simply a positive result.

The team, including Heneghan, reviewed evidence collected from 25 studies in which viral specimens from samples of positive tests were virally cultured to test whether they were able to grow. This indicates whether a positive test contains an active viral sample that is able to reproduce and transmit or just viral fragments that are dead and unable to grow either in the laboratory setting or presumably in an individual.

The diagnosis of Covid-19 involves an RT-PCR swab test as the standard diagnostic method in both clinical and community-wide settings. It uses numerous processes and chemicals that amplify the genetic material of the virus to aid its study. As discussed previously, "cycles" that occur to recover sufficient viral material to identify it could be utilised to indicate how much virus is evident. The more replication cycles needed, the more infectious an individual may be, which presents an unquantified risk for false positives. Jefferson et al. (174), suggest that while every sample cannot be cultured in a laboratory, an indication of a samples viral content could be deduced from knowledge of the number of threshold cycles required to identify the virus which could provide evidence of whether it is indeed an active infection. (175)

Gniazdowski et al. (176), suggest that even when SARS-CoV-2 was detected molecularly, acknowledgement of the number of cycle thresholds provided increased accuracy in infection diagnosis, particularly in combination with RT-PCR test results, and in those presenting with clinical symptoms. One hundred sixty-one cases indicated positive by RT-PCR exhibited a wide range of values for cycle threshold, which is suggested to reflect variance in viral load despite all sharing a positive test that confirms their status as a Covid-19 case by orthodox means.

In viral samples found to be infectious by culture study, the mean cycle threshold value was indicated to be 18.8 ± 3.4, with a median value of 18.7. In samples that could not be cultured, indicating samples to be non-infectious, a mean cycle threshold value of 27.1 ± 5.7, with a median of 27.5 was indicated.

The research found a general trend that observed an increase in cycle threshold, indicating a reduced viral load. Interestingly, the study found that some patients initially testing negative for SARS-CoV-2, received a positive result on a subsequent test, but that the follow up positive result indicated on a previously negative patient was elicited with a cycle threshold >29.5, and that attempts to recover the infectious virus via culturing these specimens indicated the samples to be negative.

Indeed, Public Health England, acting on behalf of the United Kingdom government (177), state that the cycle threshold provides a value that is semi-quantitative and able to broadly categorise viral concentration within a sample collected by RT PCR. Yet they add the context with regards to samples collected from the upper respiratory tract may be inadequately collected or represent a degraded sample. As such irrespective of the same sample being used to diagnose a case of Covid-19 disease, single same sample cycle threshold values are suggested to be unreliable, noting that values for cycle threshold are not directly comparable due to variances in assays types, not only between laboratories but also within the same laboratory which may have used multiple assays.

The United Kingdom government/SAGE stance is that around six to seven per cent of the population have been infected with SARS-CoV-2 due in part to seroprevalence studies of viral antibodies within the blood. (64), A position that is not supported by Sekine et al. (178), in an investigation of the close family members of patients with “confirmed” Covid-19 infection, finding T cell reactivity in individuals that were asymptomatic or seronegative. Approximately 60 per cent of close family members were evidenced to produce antibodies, yet 90 per cent evidenced T cell response, suggesting that many did not produce or maintain antibodies despite infection. Gallais et al. (179), also concluded that SARS-CoV-2 might induce virus-specific T cell responses without seroconversion, and that reliance upon epidemiological data based upon SARS-CoV-2 detection may be substantial underestimating prior viral exposure within the population. Media attention has maintained a focus on antibody research, and in contrast to the above findings, studies such as Long et al. (180), and Seow et al. (181), that report the waning of SARS-CoV-2 antibodies to at around two to three months fuelled a narrative in both the media and in governmental policy (64; 182), that repeat infection was a plausible risk that necessitated extreme measures to protect not only the 94 per cent that had escaped infection but the minority six per cent that had been theoretically infected already. (183)

Le Bert et al. (184), state that “T cell reactivity was found 17 years after the patients were infected with SARS, which led them to suggest the possibility that T cells generation may protect or reduce the pathology of SARS-CoV-2 infection. This would suggest that the basic premise that antibody data would allow an understanding of whom remained at risk and who was protected is inherently flawed, a fact discussed by Altmann and Boyton. (185)

In reviews (186; 187), of the primary and secondary outcome measures of phase III placebo-controlled trials, T cell reactivity is not considered. Thus, pre-existing immunity levels are not considered either in need to vaccinate previously exposed individuals or in regards to the suggested outcomes that Covid-19 vaccination is currently suggested to confer only short term “immunity”. With studies concluding at 56 days, it is currently impossible to suggest long term immunity is possible, and given that “immunity” is measured by antibodies, one must conclude that it does not look plausible given the above-noted evidence.

“Immunity” via vaccination

The known candidates for Covid-19 vaccine are Pfizer (188), Moderna (189), Johnson & Johnson (190), and AstraZeneca (191), with Pfizer's already being issued emergency authorisation in the United Kingdom at time of writing. Some degree of transparency occurred in publishing vaccine trial protocols. While worthy of praise, the protocols do raise concerns that are seemingly ignored, both by a nation seeking a silver bullet, and government looking for some semblance of success in what has to date been an unmitigated disaster.

The protocols utilised seem to have been specifically designed to prove the vaccines' efficacy, despite minimal measured effects. A trial for a vaccine would typically be expected to have a critical outcome measure, the prevention of infection. As discussed, this would need to occur alongside RT-PCR testing controlled for cycle threshold, serological tests, antibody tests, and more importantly, T cell reactivity measures.

Yet all the trials conducted did not have the prevention of infection as a criterion for effectiveness, or success. for any of these vaccines. In all studies, the primary suggestion of successful outcome was that in those with confirmed infections, the differences in symptom severity between vaccinated and unvaccinated participants were indicated as vaccine effectiveness. Thus, measured differences in symptoms amongst those identified as being infected with SARS-CoV-2 (the accuracy of which may be affected by cycle threshold) determines that the so-called "vaccines" are not effective in preventing infection, or transmission, but theoretically may be effective in modifying symptom in those classed as infected.

In much of society an expectation, and indeed a belief may be that an effective vaccine is one that not only prevents severe disease, but the transmission of the disease/virus to achieve the desired herd immunity. The trials by Pfizer and Moderna that have been indicted for emergency use authorisation in the United Kingdom at the time of writing, and the protocol used by AstraZeneca do not establish that the product prevents serious disease, just that prevention of mild-moderate symptoms are prevented or reduced.

Tests for vaccine efficacy in disease prevention, require large clinical studies that take many years and involve 30-60 thousand participants, rather than the less rigorous protocols that saw manufacturers achieve authorisation for emergency use by the Medicines and Healthcare products Regulatory Authority (MHRA), and seek emergency use authorisation (EUA) from the United States Food and Drug Administration (FDA), via their limited preliminary results.

The protocols also set out rather mild symptoms as the stated requirements for diagnosis that an individual has contracted Covid-19. Minimum criteria to be included as a Covid-19 case is a positive PCR test, which has already been discussed in regards to issues with accuracy, are either one or two symptoms including fever, headache, mild nausea, or a cough. All symptoms that are notable as common cold symptoms, side effects following vaccination and more astonishingly are amongst some of the symptoms indicated for injection of sodium chloride, which is used in the placebo vaccine. (192; 193) Criteria for approval is indicated to be the variance in symptoms displayed in control and vaccine groups that are “infected”, with no use of measures of infection between groups.

For many holding out hope that a vaccine will have an ability to both prevent infection, severe illness and death, particularly in those with known preexisting conditions, or older members of society, the vaccine is hoped to allow social interaction to occur once again. Yet severe illness and death outcomes are listed as secondary objectives. The prevention of death and even hospitalisation from SARS-CoV-2 infection are not critical to the phase III trials satisfactory conclusion.

In being deemed effective in the United Kingdom, and as is expected, in other nations, the trials conducted today have simply been set out so that products can be established as effective by measures that are presumably the lowest barriers to success. Whether this is yet again for political aplomb by a government in crisis, or simply part of an industry race to meet demand and beat the competition remains to be seen. As things stand, work remains incomplete in establishing vaccine efficacy. Questions arise as to whether such detailed research will be completed, or if this “emergency response” will become the new normal in bringing pharmaceutical to market in global pandemics.

Pandemic Parlour Tricks

As has been discussed in this text and both Consistent Eating (143), and Controlling Intuitive Appetite (124), science and particularly research remains at risk of data hacking and other scientific attempts to skew evidence to maintain a hypothesis.

As has been discussed, increased amplification or cycle thresholds have been identified as having the potential to increase false positive, to diagnose cases of Covid-19 in individuals who may not have active infections. The much fated second wave of Covid-19 in the United Kingdom saw a paradox in which “cases” grew exponentially in relation to “deaths with Covid-19”, which may have occurred due to several factors;

Increased test availability when compared to early 2020
A less lethal strain but with increased virulence
Increased cycle threshold

The discussed issue with cycle threshold provides a plausible possibility that post-vaccination, tests could be conducted with lower amplifications which would naturally lower cases by omitting positive samples that are prior infections and simply fragments of dead virus.

This effect, whilst being plausibly deniable as either “conspiracy theory”, is, in fact, possible given that numbers of cases could be dialled up and down at will via sleight of hand parlour tricks that manipulate the data to suit the desired outcome. Such underhand tactics may seem far fetched; one needs only consider previous activities both within the industrial-medical complex, and government, particularly in the United States and the United Kingdom concerning historical and recent manipulations. (7; 124)

Globally the establishment of RT-PCR testing as the Covid-19 gold standard has been flawed, indeed, without the availability of viral material, reliance was put upon the specific genetic sequence initially published by Chinese scientists (194)

Test protocols both globally and even within nations have utilised RT-PCR testing that requires two primer matches, instead of the preferred three. A potential “oversight” that may render such test protocols inaccurate in their ability to both delivery results, and in their use in comparing data against other variations of test protocols, with Borger (195), suggesting that the use of such a poor PCR test protocols, combined with a high cycle threshold (>35), as is common both in the United States and throughout Europe. Leads to a probability of infection in a positively diagnosed person is <three per cent, suggesting the probability of a false-positive result is, therefore, 97 per cent.

Even the United States own Dr Fauci is evidenced on video stating that; "If you get a cycle threshold of 35 or more…the chances of it being replication-competent are minuscule…you almost never can culture virus from a 37 threshold cycle…even 36… it's just dead nucleotides, period." (196)

As the virus apparently spreads rapidly with a drastically increasing number of cases appearing despite the introduction of many measures (masks, social distancing et cetera), many have noted that a significant majority are free from what may be classified as severe symptoms. This led to the warning initially that specific groups such as infants through to adolescents may be asymptomatic superspreaders (197). While not evidently sick, it did help transmit the virus amongst the community.

This narrative changed; specifically, it seemed to alter when the government required schooling facilities to reopen, so that the economy may also be opened by allowing parents and caregivers to outsource childcare once again. Around this period spread amongst younger people was partially dismissed as irrelevant, and asymptomatic spread was thus positioned as a community-wide problem with the potential for anyone without symptoms to spread SARS-CoV-2.

Remembering, as discussed in Controlling Intuitive Appetite (124), diseases are similar to language, and definitions alter as culture or industry manipulates its usage. Polio's apparent eradication through vaccination is due primarily to manipulating the classes of symptoms classified as polio. Jonas Salk's miracle polio vaccine is a story perpetuated in current orthodox media, particularly in light of the announcement of Covid-19 vaccine availability. Polio, a disease often linked with dichlorodiphenyltrichloroethane (DDT) poisoning. (198) Before introducing the vaccine in 1955 >50,000 people within the United States contracted polio per year, by 1955, a 45 per cent decline was evident, and in 1955 the figure was 28,985. (199)

Dr Bernard Greenberg, the head of the University of Carolina School of Public Health's Department of Biostatistics stated that; qualification for diagnosis of paralytic poliomyelitis required a patient to be exhibit symptoms of paralytic state for at least 60 days following the diseases onset from 1955 onwards. Before the availability of vaccination (<1954), symptoms needed to be exhibited for just 24 hours with no need for confirmation from either laboratory testing, or the residual presence of paralysis. Such changes in defined terms alter reporting and often lead to symptoms being attributed to other disease classifications. In 1955 we started reporting new diseases, "polio-like" illnesses such as transverse myelitis, acute flaccid paralyses, and aseptic meningitis which seem to be increasing in prevalence. (200; 201)

While some "polio" cases result in temporary paralysis, some present with no paralysis and symptoms range from fever, headache, sore throat, vomiting, fatigue, muscle aches/weakness, pain and stiffness in the back, neck or limbs, to meningitis. (202)

By redefining diagnostic criteria, this contributes to a downward shift in documented cases and a rise in other disease pathologies. Similar effects may be apparent in Covid-19 with similarity in pathology to other diseases, alterations in defined symptoms as time advances, with initial reports of symptoms for mild disease as;

Presenting with uncomplicated upper respiratory tract viral infection and may exhibit common non-specific symptoms;

fever
fatigue
cough (both with or without production of sputum production)
anorexia (medically described as lack of appetite/disinterest in food. 
malaise
muscle pain
sore throat
dyspnea (difficulty or laboured breathing) 
nasal congestion
headache

 (4; 7; 203; 204; 205)

Indeed, as documented in Controlling Intuitive Appetite (124), science seems to be for sale to the highest bidder, with industry seemingly able to pay for desirable results to be both published and receive peer review. Yet a replication crisis seems apparent when others attempt to reproduce the same results. (206)

This replication/reproducibility crisis is a methodological effect evident in numerous scientific studies and fields where the findings are either difficult or impossible to reproduce. Within the field of medicine Ioannidis (207), found that from a total of 49 studies conducted between the years 1990 to 2003, accounting for >1000 citations, 45 of the studies claimed effective therapeutic effect, yet further studies subsequently contradicted 16 per cent of the studies.

Baker (208), surveyed>1,500 researchers, with >70 per cent stating they had attempted to reproduced the experiments of other scientists and failed to replicate the findings.

Again Ioannidis (209), highlights this problem, suggesting a need for research to become patient-centred, rather than focusing upon the “needs of physicians, investigators, or sponsors.” Despite this crisis in academia, and the industrial pace at which Covid-19 research occurred, both under time pressures, but free from formal peer review, we are told the government are following “the science” and that we should trust the experts.

Scientific credibility is achieved by research and by establishing further with evidence via their replicability with newly acquired data. This stands alone from retesting scientific “evidence” using the same data and analyses (reproducibility), and retesting existing data with various types of analyses (robustness), in such situations outcomes that were consistent with the prior findings increase confidence, and inconsistent results decrease the confidence.

In Covid-19, it seems there is no exact replication occurring in testing and diagnosis, with every test potentially utilising different cycle thresholds amongst other factors such as assay variability. As such generalisability in data decreases the confidence in the findings as the potentially unique conditions applied to RT-PCR tests can not be considered a replication study.

The inability to validate the test data to support either the number of presenting cases, or the much-queried number of deaths “with Covid-19” (remember that preventable deaths should indeed be considered tragic losses, even if not due to SARS-CoV-2), skewed data does not present an accurate picture of either the scale of the problem, or whether measures are appropriate or effective.

This coupled with the suggestion that antibody production remains low following infection, a process entirely expected in younger and or “healthy” populations that rather than diverting energy generation to a complex, slow and energy-intensive process of antibodies production, utilises what is termed the innate immune system, which works via a far more efficient process involving T-cells that defend against future infections. A such, one would expect to see little or no evidence of antibodies as timespan progresses. Its use by SAGE to guide the proportion of infection amongst the population is either an error due to inadequate qualifications amongst a SAGE team primary constituting mathematicians, modellers and behaviourists, with a government also lacking in biological knowledge. Or due to some degree of malice by those seeking to maintain an unproven narrative that is undoubtedly failing.

Estimating SARS-CoV-2 infection rates within the United Kingdom population may be achieved using the known infection fatality ratio (IFR), which is imperfect, given that deaths with Covid-19 may still be falsely positive. However, theoretically, this is less problematic than the opposing stance of utilising antibody data in all cases, including those codified asymptomatic.
Despite government confidence, the current policy leaves us with this "known unknown" that both seriously hampers understanding of the crisis and damages that response. This effect has been seen by many as the pandemic rages in. The Imperial College team (38), led by Professor Ferguson, suggests that <7 per cent of the United Kingdom population have been infected, which powerfully justifies prolonging lockdowns, social restrictions, and early vaccination rollout. Relaxation of measures such as social distancing are suggested to risks millions of individuals becoming infected, and the already depleted national health service becomes overwhelmed, as it does each winter. (210)

The model suggested excess deaths of circa 510,000 without precautions, and approximately 250,000 using a mitigation strategy, dropping to 20,000 if the plan was to suppress the virus. This suggests that a policy of lockdown would prevent 230,000 excess and unnecessary deaths occurring.

As this paper has sought to establish, the model propagated by Professor Ferguson seems to have drastically underestimated infection rates amongst the population. A paper by Lourenço et al. (211), led by Professor Gupta from Oxford University, suggests that various estimates are suggested for a percentage of infected (both current and prior) population within the United Kingdom, with figures as high as 68 per cent. Critics claimed that Professor Gupta's work was too "speculative" with little "empirical justification", yet the Imperial model also falls foul of the same accusation. The previously discussed estimates are based upon assumptions built into the Imperial model, which created an implausible view of a novel virus. One would assume that models could be updated and coded to work with newly available data, such as cycle thresholds for RT-PCR tests (for example >30 cycle threshold positive tests could be weighed more towards being indicative of prior infection), T-Cell reactivity et cetera.

Being able to increase the accuracy in gauging rate of infection helps not only guides and justifies policy interventions but helps to establish the infection fatality rate (IFR) which is vastly different from the case fatality rate (CFR), that uses the number individuals that tested positive (ignoring false positive and negative results) and is divided by the total deaths (ignoring questions about whether SARS-CoV-2 was the specific cause of death or a co-factor). Variability in CFR occurs between country due to multiple variables, including testing availability et cetera.

Ioannidis (212), led a team to assess the actual infection rates in Santa Clara County, California, using serology testing for antibodies, which as noted performs poorly in documenting longterm exposure rates, specifically in younger/“healthier”. The team looked at the data of 3,300 Santa Clara County residents in the United States and found rates of infection to be 50 to 85 times the amount of cases officially documented (956 at the time of the study).

Loss of antibodies, while biologically expected due previously explained reasons (antibodies production is energetically expensive, while T-cell reactivity which is part of innate immune function is less so), is suggested as a reason for caution within communities (lockdown et cetera) do to the “known unknown” regarding whether re-infection is plausible. (213)

A Japanese woman (214), was suggested to have been re-infected but was classified as being “immunocompromised.”

In considering this we must rationalise many aspects, firstly considering the terms, being classified as suffering from Covid-19 may not necessarily be due to being evidenced SARS-CoV-2 as was clear early in the pandemic within many nations, diagnostic testing was not available to many, as such symptoms were utilised and quarantine necessary. It must be noted that such symptoms are shared by many other pathologies, including the common-cold, which of course can be due to specific coronaviruses. We must also differentiate between the two actual positive results; one may indicate a live virus evident by an RT-PCR utilising a low cycle threshold. The second may be a test procured due to the onset of similar symptoms and the positive result produced using a much higher cycle threshold. Without the availability of data on test protocols, we can not accurately consider whether reinfection is plausible. Indeed, in a case report by Prado-Vivar et al. (215), they put forward evidence including epidemiological data, clinical findings, the positive RT-PCR re-test, two different virus clades and the antibody response as being compatible with reinfection, but admit a critical limitation of the study was the failure to culture the virus, as such we are unable to conclusively state whether it was reinfection to fragments of prior infectious viral material that is no longer live or presenting a risk to others.

Viruses do mutate, and as noted tend to become more easily transmissible, but less dangerous. As discussed, it is implausible that as suggested by the Ferguson Imperial College model, that it presented a novel pathogen. The nature of evolution means it has ancestors and will continue to do so. However, our exposure to one strain should confer some immunity to further, specifically weaker strains. Access to cycle threshold data and T-Cell reactivity studies could re-code the current epidemiological models and provide better-guided governance and strategic planning in tackling the virus, restoring public confidence and creating a plan that allows the economy to reopen. Without such data, and in the hands of leadership relying upon so-called super-forecasters (216), the country seems destined for regular lockdowns and cyclical vaccination programs to “protect” against reinfections of new strains. Undoubtedly, the country (and many other nations) are in the grips or a pandemic that is straining health care provisions beyond their capabilities, but it is essential to gain context. In the United Kingdom, austerity and poor management have not only limited the resources of the National Health Service, which is annually at breaking point each flu season, but staffing levels have suffered due to insufficient funding for students aiming to enter the health care industry, and poor retention of staff due to wage freezes and poor working conditions. 

In Controlling Intuitive Eating (124), I wrote that intelligence might be better measured by the ability to observe, analyse, and update beliefs. At this, we are failing, while an emerging pathogen causes fear and reactionary strategies, as timespan increases “the science” could and should be updated rather than moulded to fit the policy. That this continues alongside issues of cronyism in government contracts for personal protective equipment (PPE), testing, and vaccination causes a further degree of distrust in the political strategies utilised to date.

Science needs to be utilised to its full capacity, not coopted to justify policies that meet industrial and political desires.

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​

From around 1999-2004 milk was a major part of my diet, some might say that my increased consumption (I'd always been a fan) was a factor in my incredibly high metabolism during that period (for those that are unaware, you may wish to seek out my articles and podcasts discussing my 6000 kcal intake). For those that are fans of the work of rebellious scientist and philosopher Dr Ray Peat, the milk consumption coupled with my jelly sweet consumption, love of coffee and general carbaholic status gives good evidence of the effects of a so called "peatatarian" diet.

Whilst I had an awareness of Ray via my studies of Broda Barnes, I had yet to fully immerse myself in the Fan Girling whirlwind that encircles Ray...although he is totally unaware of his celebrity status. What happened next was a few years of hell that eventually brought me full circle and ensconced me in Ray's work. A place that not only felt comfortable and reassuring, but a place that reaffirmed how close I'd been way back when. It showed me that my time in the whacky paleo/metabolic typing/CHEK world was damaging but the ultimate experiment/lesson.

And so it came to pass that I once again began consuming milk (I gave it up during faileo as I couldn't get raw pasture raised). And with it I returned to my milk powder bake. As ever it was a Ray statement about milk powder pancakes that sparked the memory, so I adapted my recipe to use his ideas, but baked it my old way rather than frying in a pan.

Enjoy



Ingredients

1 cup of milk powder (I use Organic Skimmed)
1/3 cup of Milk (I use Organic Skimmed)
2-3 tablespoons of sugar
1 egg

Directions

Mix all the ingredients in a bowl to a smooth consistency. Pour into a dish that is suitable for the over (I use the glass lid from a casserole dish)
Bake in the oven at 180-200 degrees C for around 15-20 mins, or until golden brown. Around 10 minutes slice a cross to allow the inner part to cook.

Serve with Greek yogurt, cream or Ice Cream

Over the Christmas period I suffered at the hands of a PayPal reverse transaction, I've had the odd occurence of being scammed in the past. From my agreement at Virgin Active to be repaid for a training course if I remained working at the company for a year (they blamed a change of finance team), through to a someone promising to pay me for some lab tests that I'd paid on their behalf.

I've long ago accepted that people will try and take advantage and as with life you have to take the rough with the smooth, but I always hoped I had the support of the company I used to accept payments, PayPal. Sadly it didn't work out that way, and over Chrismas I suffered a loss due to someone reversing subscrition payments. I'm not in this work to become a millionare, I value my time and my research more than profit as most will tell you. If it was about the money I'd work at GloboGym, sell a preprinted diet sheet, or work in the NHS.

The idea behind the subscription service was to allow users to access myself at a reduced rate for brief interactions by email (giving you priority in my email box), and to give you access to the members section which was password protected. My blog has 300+ free posts but the members area was targeted towards the needs of those subscribed. It also contained my database of 6000+ research articles catorgorised into differing health issues that made it easy to search for relevent material. It is also the only area I made video and audio content avaiable (TV and radio shows I've been part of, plus my own recordings) as I'm not too keen on this type of media and prefered it kept away from open viewing. The members area started from what was initially a "school" area, in which I trained numerous individual who worked in a variety of health releated jobs. Three years ago I opened it up to subscribers well aware that people would make copies and share my work. Yet I didn't expect to be quite this exposed.

PayPal state their terms to be;

11.10 What are examples of items/transactions/cases that are not eligible for PayPal seller protection?

1. Intangible items, licenses for digital content, and services.
2. Items that you deliver (or are picked up) in person (except for items for which you received payment through the PayPal Location Based Payments Functionality).
3. Transactions made through Zong, Website Payment Pro (PayPal Direct Payment and Virtual Terminal).
4. Claims, Chargebacks and Reversals for Significantly Not as Described; and/ or claims filed directly with eBay.
5. PayPal Business Payments.

So despite having spent a few days over Christmas attempting to protect my work, I have no option other than to suck it up and wait for PayPal to unblock my account. I've always viewed my independent research as an artistic outlet, so to have someone potentially use it, copy it, distribute it, then be able to gain a refund doesn't feel great.

As of today my site will run via stripe rather than PayPal which hopefully won't cause you any difficulties. I have also shut down the members area, stopped taking subcriptions and refunded those that were current members. My plan is to gradually transfer some of the work to Patreon, but as I'm sure you will appreciate this will mean reformatting and editing content to make it suitable. 

Thank you to all my supporters, I'm sorry to make these changes but hopefully Patreon will work out and I'll get more time to dedicate to my research/book. As ever, I'm available for consults via my store.

The Christmas binge season is creeping up on us, and as ever it will be quickly followed the annual tradition of starving oneself as a penance for your syns (I know it's sins, I just borrowed a slumming world term). Metabolism is the basis of both my work and research, and it never ceases to amaze me how misunderstood the topic is.

I thought we’d look over an old article from the Daily Mirror. Not exactly PubMed but it is where most people will go for “expert opinion” once New Years Eve is in their hazy past. The article by Tanith Carey was titled “How many calories do you REALLY need to eat every day? We put six women to the test.” (1) In the article they want you to consider why some women can eat anything and not gain weight, whilst others gain weight just by looking at a piece of cake. Now that simply isn’t true, everyone has the potential to gain weight, our ability to survive thus far is most likely due to our ability to down-regulate our metabolism and store energy in order to survive periods of famine. (2, 3)

The article goes on to mention the dreaded NHS guidelines that the average female needs 2,000 calories a day. The problem is how we define average female. 
Scientifically we know that we are individuals, and to use the term “average” is beyond useless, indeed, to follow some dictated policy shows an utter disregard for your individuality. With the scientific tools we have at our disposal we no longer need to conform ourselves to the system, we can define our own systems.

The article does touch on the number of calories “we can eat” varying from woman to woman. They then went onto measure oxygen inhalation and carbon dioxide exhalation to enable the calculation of resting metabolism in six “individuals. Dr Naufahu stated “As we get older, our metabolism tends to slow down, so unless we keep up our muscle mass with exercise, those extra calories get stored as fat, which is why so many middle-aged women battle with their weight.” Personally it leaves me astonished that no mention is made of food sustaining the metabolism, I've completed enough study over the years to conclude that you'll struggle to maintain or increase muscle mass without adequote food. As you'll see, metabolism seems to suffer most at the hands of the lieflong dieter.

One of those tested was a personal drainer called Jo who was 53 at time of publication, and needed 1,600 calories despite eating 1,942. Her various admissions; 

“For most of my life I’ve yo-yo dieted.….In my teens, I lost the weight through dangerous crash dieting. But then I married and gained more pounds with each of my pregnancies until I went up to 15st….”

“I started exercising and eating no more than 1,200 calories a day. It took 22 months for me to lose five stone….”

“Now I’m happy with my body and keep my figure trim with exercise and eating healthily during the week – fruit, protein and salad but indulging at the weekends. I am particularly partial to red wine…..”

“The weight still comes off much more slowly than it used to in my younger days.”

This really sums up the metabolic adaption created by dieting or making incorrect assumptions about what your body needs in terms of its energy requirements.


Further into the article Dr Naufahu’s makes a childish error when she states that "To lose a pound of fat, you need a calorie deficit of 3,500-kcals each week.” She then states that Miss Average needs to cut down by 400 to 500 kcals a day. Yet the belief that a 3,500-kcal deficit will result in one pound of weight loss (about 0.45 kg) is misguided if not corrupt. It continues to be cited in “over 35 000 weight loss educational websites” plus copious amounts of academic textbooks, scientific articles and so called experts in diet and nutrition. (4) Even the British Dietetics Association pushes the totally unreferenced 3500-kcal rule. (5) Even if it was factual it fails to account for the metabolic adaption caused by dieting. To put it simply, the greater the degree of energy restriction to encounter, the more efficient you become as energy output is slowed to protect you. (6)

Then we meet Nicola who is 54 and eats 1,800 calories despite her RMR being 1,497, interestingly she claims to .

“eat more than half what I used to in my 30s and find it harder and harder to keep it off, especially since I turned 50."

“I had a hysterectomy at 42 and have been on HRT ever since. I think that keeps me heavier because it makes me suffer water retention."

“It’s very frustrating because I don’t eat a lot. I start the day with an omelette and have lots of fish and salads – with the odd cereal bar thrown in as a treat.”

So we can see the daily recommendation based on the “average woman” are pretty much worthless, and that random dieting seems to have often detrimental effects on the Resting Metabolic Rate (RMR). The next stage up from this guesswork would be predictive equations such as Mifflin-St Jeor, (7) which I used during my MSc dissertation due to the costs involved in utilising more accurate methods across a large study group.

Their can be no doubting that predictive formula provides a greater degree of individual understanding when developing and evaluating a nutrition plan, yet predictive equations may effect longterm outcome due errors in accuracy.(8, 9) Oshima et al, (10) concluded that indirect calorimetry was an important tool for nutritional therapy of patients, so it would seem logical to conclude that those looking to lose weight (often for health reasons) should utilise the best possible tools available to enable both long term success and evade future health problems. 

That studies such as Fothergill et al, (11) describe poor weight-loss maintenance at 6 year follow up, coupled with RMR suppression, indicates the importance of knowing individual RMR in order to maintain health and longevity whilst attempting to attain weight-loss goals. (12) Whilst costs may seem prohibitive it must be noted that during a study funded by Weight-Watchers, 5 year weight-loss maintenance was reported as 16.2 percent. Whilst this seems to make it plausible it must be considered that by the studies own admission the participants were made up of only the most successful members, and is no indication of actual success rates amongst all all members. It is also worth pointing out that the study was looking at “success” measured in terms of members who managed to maintain 5 percent of their weight-loss over 1, 2 and 5 year periods. Ask yourself would you really be happy being one of the 16.2 percent in an elite group that after 5 years had managed to maintain only 5 percent of your weight-loss? Thought not.

So, at the cheapest rate for online access you’d be paying £122.68 for a year, right through to £325 a year to attend group meeting.(13) Cheap enough to risk it for those unaware of their chance of “success” and a great business model for repeat customers tricked into thinking their outcome was due to poor willpower.

So how would I tackle the issue of weight loss?

Firstly you need to know your own energy requirements, not those of Miss Average. 

Option 1. Select a formula, work out your RMR and add on your activity to give you a better estimation of your needs.

Option 2. Book in for an RMR test and gain a more accurate picture of your needs.

After completing option 2 I would then suggest (or I do it for you if you visit me) that you complete option 1 to see how your actual RMR compares against what standardised formula suggests you need.

Next you need to consider the fact that after most RMR tests are completed the individual is then subjected to the 3,500 calorie deficit rule. We already know this isn’t backed up by evidence, and cannot work long-term due to metabolic adaption. So my suggestion would be to eat the amount your body needs and begin to restore your youthful metabolism. If you are supplying the correct amount of energy you will benefit from not needing extreme willpower, and over time you’ll see the RMR begin to raise as the metabolism adapts in response to the consistent supply of energy.

Any questions, leave a comment.

References:

1. Carey, T. (2013). How many calories do you REALLY need to eat every day? We put six women to the test. 
http://www.mirror.co.uk/lifestyle/health/how-many-calories-you-really-2161639 published 14 Aug 2013 and updated 27 Jun 2016

2. Galgani, J., & Ravussin, E. (2008). Energy metabolism, fuel selection and body weight regulation. International Journal of Obesity (2005), 32(Suppl 7), S109–S119. http://doi.org/10.1038/ijo.2008.246

3. Mattes, R, D., Pierce, C, B., and Friedman, M, I. (1988). Daily caloric intake of normal-weight adults: response to changes in dietary energy density of a luncheon meal. Am J Clin Nutr, 48(2):214-9.

4. Thomas, D, M., Martin, C, K,. Lettieri, S., Bredlau, C., Kaiser, K., Church, T., Bouchard, C., and Heymsfield, S, B. (2013). Can a weight loss of one pound a week be achieved with a 3500-kcal deficit? Commentary on a commonly accepted rule. International Journal of Obesity (2013) 37, 1611–1613; doi:10.1038/ijo.2013.51; published online 30 April 2013.

5. BDA Food Facts Sheet https://www.bda.uk.com/foodfacts/Want2LoseWeight.pdf accessed 20th December 2016.

6. Luke, A., and Schoeller, D, D. (1992). Basal metabolic rate, fat-free mass, and body cell mass during energy restriction Metabolism - Clinical and Experimental , Volume 41 , Issue 4 , 450 - 4566. 
7. Mifflin, M, D., St-Jeor, S, T., Hill, L, A., Scott, B, J., Daugherty, S, A., and Koh, Y, O. (2005). A new predictive equation for resting energy expenditure in healthy individuals. Am J Clin Nutr. 1990 Feb;51(2):241-7.

8. Frankenfield D., Roth-Yousey, L., & Compher C. Comparison of predictive equations for resting metabolic rate in healthy nonobese and obese adults: a systematic review. J Am Diet Assoc. 2005 May;105(5):775-89.

9. Aliasgharzadeh, S., Mahdavi, R., Asghari Jafarabadi, M., & Namazi, N. Comparison of Indirect Calorimetry and Predictive Equations in Estimating Resting Metabolic Rate in Underweight Females. Iran J Public Health, Vol. 44, No.6, Jun 2015, pp.822-829

10. Oshima, T., Berger, M, M., De Waele, E., Guttormsen, A, B., Heidegger, C, P., Hiesmayr, M., Singer, P., Wernerman, J., & Pichard, C. (2016). Indirect calorimetry in nutritional therapy. A position paper by the ICALIC study group. Clin Nutr. 2016 Jun 22. pii: S0261-5614(16)30142-X. doi: 10.1016/j.clnu.2016.06.010. [Epub ahead of print]

11. Fothergill, E., Guo, J., Howard, L., Kerns, J. C., Knuth, N. D., Brychta, R., Chen, K. Y., Skarulis, M. C., Walter, M., Walter, P. J. and Hall, K. D. (2016), Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity, 24: 1612–1619. doi:10.1002/oby.21538 

12. Rizzo, M, R., Mari, D., Barbieri, M., Ragno, E., Grella, R., Provenzano, R., Villa, I., Esposito, K., Giugliano, D., & Paolisso, G. (2005). Resting Metabolic Rate and Respiratory Quotient in Human Longevity. The Journal of Clinical Endocrinology & Metabolism 2005 90:1, 409-413

13. Weight Watchers Pricing structure. Accessed 20th December 2016 https://www.weightwatchers.com/uk/weight-loss-plans?

From an early age I was acutely aware that life appears to be about social conformity, that we change in response to either physical or imagined pressure to meet the expectations of the group, we yield to the perceived social norms (1). It always seemed odd (and still does) that we agree to do things we'd rather not to in order that we fit in with the perceived desires of the majority (how can we be sure the majority aren't all agreeing for the same reason), so that we can fit in and be liked by the group. In effect we take our role in society in order to claim our identity and make sure other like us.

Three differing types of conformity seem to occur:

Compliance, Internalisation, and Ingratiational

Compliance occurs when our behaviour adapts in order to gain approval and/or avoid disapproval by conforming. (2) For example you may take part in bullying behaviour, or sing at a karaoke night to conform with the group, despite not actually agreeing with it. This can happen at all levels, from agreeing to those drinks you'd rather not have,  trying smoking when you really didn't want to. Right through to agreeing to bombing another country when you really don't think we should (I think with most politicians  they are most likely careerists that internalise or identify as discussed below).

With internalisation we genuinely accept the group norms because of reward. Kelman (2) states that this is high level conformity due to the group beliefs becoming part of the individual’s own beliefs, therefore the behaviour tends to become permanent. Sherif (3) found that people conform to the group norms when they are unsure, as such this tends to occur when we view the group to have authority over us. We yield to the super knowledge, as an example I see numerous clients that comply with their Doctor despite being either unsure or unhappy with the advice. We might conform to government policy on health and nutrition because the authority said that saturated fat was dangerous and polyunsaturated was healthy. We may not have the knowledge to challenge authority, and under the belief that we are rewarded with health we genuinely accept the belief. 

Identification happens when we want to establish a relationship with a person or a role within a group, (2) as displayed in the Zimbardo Prison Study in which those involved in the experiment as prison guards complied to the perception of the role. Do we comply in our role as the fat, sick and stressed once we assign ourself that identity? Take genetics, if we are fed the theory that we are genetically predisposed to a condition do we accept or even manifest it to maintain our identity. I see a lot of this on Facebook within health groups set up to supposedly support others, typically it becomes a battle to fit in and be the best/worst case.

So why do we conform? As I discussed earlier I was acutely aware of social conformity from an early age, in fact I began to suspect that extroverted and introverted personalities were often simply differing degrees of conformity. Whilst I'm typically classed as an introvert I often felt it was simply the fact that I'm more than happy to say no. My desire to be myself and do what I want tends to create the appearance of an introvert, in reality I know my own mind and won't agree to conform, not even to authority if I can prove them wrong.

Deutsch and Gerrard (4) discussed Normative and Informational conformity. Normative being the desire to fit in with group for fear of rejection despite privately disagreeing with the group. Taking drugs or getting drunk when you'd rather not out of fear that you'll be ostracised from the group is a good example, and one that most people can relate to. Informational conformity is when we lack the knowledge and look to the group or authority, usually we then adopt this behaviour as our new norm. This often seen in the health industry, from dieters following diet gurus, happy to accept preprinted diet plans, spending cash on yet more editions of the blobby coaches mean in 15 books. Right through to our acceptance of government and scientific/industry policy without question. The promise of reward (skinny/health) in response to submitting to the group ideology has us conforming with something purely based on trust. Two of my friends are soon to release a long awaited documentary that I backed via kickstarted called "On the Back of a Tiger".(5) The film looks at the work of a group of renegade non conformist scientists and considers the conformation for industry rewards that is rife in the scientific community, this will also be the topic for my next blog.

• So what makes some of us fail to conform to the social pressure?
• What makes a freethinker think for themselves?
• Are we taught conform?
• Does public policy on food and drugs help with conformity? Are we drugged droids?
• Is freethinking a risk to the authority/ruling class?

All these will be covered in up and coming posts, but please feel free to comment below and add your voice to guide future posts.

As you may of noticed some of my post have started going via Patreon, the main reason for this is due to my desire to remain independent and not conform. Some of you may know that the previous year has seen a battle with three Universities who have all been keen to explore my research. Yet at the final hurdle I have time and time again failed to secure PhD funding when I refused to alter my proposal to conform. Two academics privately praised my intention but stated that the institution receives funding from industry that opposes my ideas. 

I will not climb on the back of the tiger simply to gain acceptance and would rather go it alone. Patreon isn't expensive and my ultimate plan is that rather than purchasing a small online consult with me (currently £8 a day, £30 a week) you will use Patreon at a much cheaper price and the questions will be answered (maintaining your anonymity) in a group post which enables you all to see the Q&A's.

All the monies generated from this method will go towards furthering my research, and it is my intention that the research will be transmitted live so that you can make suggestions, ask questions and generally get involved.

References;

1. Crutchfield, R. (1955). Conformity and Character. American Psychologist, 10, 191-198.

2. Kelman, H. C. (1958). Compliance, identification, and internalization: three processes of attitude change. Journal of Conflict Resolution, 2, 51–60. 

3. Sherif, M. (1935). A study of some social factors in perception. Archives of Psychology, 27(187) .

4. Deutsch, M., & Gerard, H. B. (1955). A study of normative and informational social influences upon individual judgment. The journal of abnormal and social psychology, 51(3), 629.

5. The Production Journal for: On the Back of a Tiger​. Perceive Think Act http://perceivethinkact.com

References:

1. Cerqueira MT, Fry MM, Connor WE. The food and nutrient intakes of the Tarahumara Indians of Mexico. Am J Clin Nutr. 1979 Apr;32(4):905-15. PMID: 433816.
2. http://raypeat.com/articles/nutrition/carrageenan.shtml

Ingredients

• 75g Masa Harina
• ¼ tsp salt
• 2 eggs
• 200ml whole milk
• 75ml water
• 50g refined coconut butter​ (you can use normal butter)
• 50-100g of sugar depending on how sweet you'd like them. 

Makes around 6-8 pancakes

Perfect with squeezed orange juice and either maple syrup or sugar sprinkled on top. A personal favourite is strained Greek yogurt or ice cream with stewed apple.

1. Place the masa harina, sugar and salt into a mixing bowl, making a well in which you break the the eggs into. Scramble the mix and then add both the milk and water.
2. Mix till you have a smooth batter.
3. Use 2 tbsp of butter in the batter and continue to mix.
4. Heat a frying pan over medium to high heat. Drizzle a little melted butter in the pan before adding 2 tbsp batter. Circle it round so that the batter spreads evenly.
5. Cook till golden brown underneath before flipping and cooking the other side.
6. Repeat as desired or store the batter in the fridge for use another day.
7. Add your toppings and enjoy.

Doctors have patients I have...people, friends, I don't know what else to call them? They're just people that ask for help, maybe because they read my blog, saw something I posted on Facebook or somebody suggested they chat to me. From my very beginnings in they health industry I hated the word patient. At one point I had a desire to become a Doctor, with one or two caveats, I neither wanted patients nor did I want to dish out pills in an authoritative manner without the "patient" being involved in the diagnostic process. Hence I didn't get past the Med School interview and I'm not a Doctor.

My love of diagnostic processes, a desire to collate data prior to making an informed decision, and the above all that I present my findings to the individual, explain the differential diagnostic process and allow them to draw their own conclusions. It is important that I do not diagnose, partly because I'm not allowed to as I've not ticked the right boxes and attained the correct title, but more importantly because nobody should be a greater authority then the person themselves.I meet two types of people in my work, the anti-authoritarians and the patients. The patients typically struggle with my methods, they want me to be the authority, I want them to fix themselves (with some guidance). They want a diet sheet, I want them to learn, to understand, to take ownership, to realise that things change. And that unless they take the wheel, they may veer wildly off course without even realising it. 

authority NOUN

The power or right to give orders, make decisions, and enforce obedience.
‘he had absolute authority over his subordinates’
‘a rebellion against those in authority’​

I got the poison.
I got the remedy.
I got the pulsating rhythmical remedy.
I got the poison.
I got the remedy.
I got the pulsating rhythmical remedy.
I got the poison.
I got the remedy.
I got the pulsating rhythmical remedy.
I got the poison.
I got the remedy.
I got the poison. I got the poison. I got the poison.
Yeah... Yeah... Yeah...
Yeah... (Boom...) Yeah... (Bah...

We turn up our noses and sneer at those dastardly low-life drug addicts that blight our society. They've got the poison and we think we know the remedy...abstinence, therapy or better still, a criminal record. Yet our streets are lined with Starbucks and Pubs, they're legal and we love it. So why when the worlds most popular drugs are street legal, do we hold such disregard for those seemingly "addicted" to less socially acceptable (depending on the circles you move in) drugs such as heroin or meth?

Are we better addicts? Do we deserve to live a better life? To be loved despite our self-medication? Their can be no doubt that suffering is a part of life, and our ability to adapt to this is what shapes us. Yet their can also be little doubt that  "addiction" is a form of suffering, and that If we attach the tag "addict" because you have a beer or bottle of wine every night, does that increase the belief that you need the substance and that you're suffering an infliction?  Addiction may not even exist, it may just be a biological response to some sort of suffering, a way to numb the pain, be it physical or emotional. Bang your knee and you'll self-medicate by rubbing it better. Starve yourself of food or a particular macronutrient under the guidance of any number of foodie/nutritionalists and you're likely to self-medicate with any number of "treats" when it all gets too much. You may label this an addiction, a cheat day, call it flexible dieting or even ignore it and promise to get back on the wagon tomorrow.

In the 1970's Dr. Bruce Alexander ran his now famous Rat Park experiments, tracking white laboratory rats housed in cages in close proximity to one another,  separated by the steel sides, only engaging in contact when lab staff brought food, water etc, basically solitary confinement. At other times they suffered prolonged starvation and were confined to skinner boxes which allowed for punishments and rewards (limited feeding and electric shocks etc). Inside the skinner boxes the rats reward themselves with pellets by pushing a lever on the side of the box. The metal allowed for administration of electric shocks in order to punish rather than reward. Eventually they considered addiction, and the rats were allowed to inject drugs by pressing the lever, a process that involving being tethered, cathetered (to allow the drug to enter the bloodstream). The results showed that the rats continued to use the lever to self administer heroin, morphine, amphetamine, etc. Thus it came to pass that drugs were labelled addictive to rats and naturally to humans as well. And so began the War on Drugs, and with it, harsh retribution for anyone caught with anything not allowed by the authoritarian state. 

Alexander however realised that rats are highly social, and that solitary confinement may drive them crazy which may increase the desire to self-medicate. He also realised that while isolated they had no real options, they couldn't escape the cage and pushing the lever if for no other reason than to stem the boredom seemed inevitable. Along with colleagues he undertook studies to compare the drug usage of rats in a fairly normal environment versus those in isolation. To do this he built a park environment filled with things to climb on, hide in, other rats (of both sexes) and adequate nutrition. Pretty much every experiment they ran showed that the isolated rats consumed more drugs no matter what variables they ran.

Despite the findings being replicated by other researchers it was largely ignored, and continues to be to this day. Addiction is an irresistible disease, something we're all susceptible to, something is claimed to have genetic risk factors. Is it too profitable to turn our backs on expensive long-term drug treatments and therapy, when it may be more useful to consider the socio-economic environment? Why do human become "addicted"? Do things make us feel caged or isolated?

Alexander went further, sadly he couldn't conduct Human Park studies due to ethical reasons, but he was to look back at historical data. Such as when our ancestors colonised various native tribes in Western Canada during the 18th and 19th century. The natives were broken, both economically and culturally, losing their homes and being forced to abandon their language. History shows us that alcoholism became rife, which was explained by the settlers as genetic vulnerability. In effect the natives were the rats, isolated, forced into a new culture and basically caged in an environment that they didn't wish to be in.

What causes your "addictions"? Do you need that wine to numb the pain of working in a job you detest? Is that drug addict that you look down on really just numbing the social and economic pain of being isolated in an environment that basically leaves them with no obvious way out. Are your food issues caused by the likes of Joe Wicks, Davina McCall, Weight Watchers or any other diet club or guru caging you in an environment that leaves you undernourished? Is Jamie Oliver freaking you out about sugar, causing you to create a cage in you restrain yourself from consuming an important fuel?

Are your addictions due to a cage that you have created for yourself? Or even one you have let someone create for you? It's time to escape your cages...

The news that "more than 170,000 people in the UK who were diagnosed with cancer up to 40 years ago are still alive", is a positive step forward suggests Macmillan Cancer.[1] Apparently "people are twice as likely to survive for at least a decade after being diagnosed than they were at the start of the 1970s". This it is suggested is due to better treatments and diagnoses. The report [2] Cancer Then and Now, suggests that long-term issues are a major factor in 'survival' and I would suggest that these long-term issues may become a factor in the future.

I've previously written about the "war on cancer" [3] and the statement from Macmillan just doesn't sit well with me;

"People are now twice as likely to survive at least 10 years after being diagnosed with cancer than they were at the start of the 1970s"

For a start, the statement is referenced with the Quaresma, Coleman, and Rachet's (2015) study, in which the assessment of progress in cancer control was based upon an observational study. In "patients diagnosed in 1971-72, the index of net survival was 50% at 1 year after diagnosis. 40 years later, the same value of 50% was predicted at 10 years after diagnosis."

"Predicted 10-year net survival adjusted for age and sex for patients diagnosed between 2010 and 2011 ranged from 1·1% for pancreatic cancer to 98·2% for testicular cancer."

"Net survival for the oldest patients (75-99 years) was persistently lower than for the youngest (15-44 years), even after adjustment for the much higher mortality from causes other than cancer in elderly people."

"The very wide differences in survival for different cancers, and the persistent age gap in survival, suggest the need for renewed efforts to improve cancer outcomes."
FUNDING: Cancer Research UK.

Further into the report, they "estimate that at least 170,000 people are living with cancer who were diagnosed in the 1970s and 1980s." 
Despite all these estimates, the death rates among adults seem to be steadily rising other than when you jiggle the figures and use age restandardisation, a point Ray brought up previously in his article on Breast Cancer. [5]

"Government officials, editors of the big medical journals, professors and broadcasters, have been able to get away with this huge statistical fraud. I suspect that they will soon feel encouraged to simply make up the data that they want, because eventually “age standardization” isn’t going to work to hide the actual increases in mortality. Since people with cancer usually die of something else, such as a stroke or heart failure, it will be no trick at all to make cancer mortality decline to be replaced by other causes of death. The precedent for such fabulizing of data exists in the FDA’s approval of AZT, and other less notorious drugs." - RP

​Whilst I'd like to bring the news that the headline is full of bright prospects, it is seemingly a propaganda piece aimed at keeping us focused on fighting the war on cancer. To keep morale high and convince us that we are succeeding. As I've stated previously, unless mainstream science admits some huge failings, the war will continue.   

​1. Cancer: Thousands surviving in UK decades after diagnosis http://www.bbc.co.uk/news/health-36925974

2. Macmillian Cancer Then and Now report http://www.macmillan.org.uk/documents/campaigns/cancer-then-now-report-final-online.pdf

3. Craig, B. War on Cancer http://www.billycraig.co.uk/blog/war-on-cancer

4. Quaresma M, Coleman MP, Rachet B. (2015). 40-year trends in an index of survival for all cancers combined and survival adjusted for age and sex for each cancer in England and Wales, 1971-2011: a population-based study. Lancet. 2015 Mar 28;385(9974):1206-18. doi: 10.1016/S0140-6736(14)61396-9. Epub 2014 Dec 3 http://www.ncbi.nlm.nih.gov/pubmed/25479696

5. Peat, R. Breast Cancer http://raypeat.com/articles/aging/breastcancer.shtml

I started writing this post pre European Union (EU) Referendum, and I never intended it to become linked. However, after Brexit brought about a surge of nationalism that allowed casual racism and xenophobia to rear its ugly head, I realised things really haven't changed that much in regard to our love of eugenics, although we now prefer to call it plain old genetics. It was also the biggest factor in my desire to remain in the EU, before you say it, I know I know, not every leave voter is/was racist. I just happen to have spoken with a great number of individuals who can't put forward any other reason, except "keeping them out", "we've got to look after our own" etc. Their were some who claimed that we had a bad deal (most couldn't specify why), but now we have no deal and a great deal of unknown till we find out exactly what the new deal is. Lot of deals there, but thats the way it is, and I'd be willing to place a bet on our deal being somewhat worse than we intend to leave behind. We'll no doubt still have the immigrants that upset Nigel, but what about the things we stand to lose? 

In the 1880s Sir Francis Galton concluded after studying the upper classes that their social standing and superior prospects were due to better genetics in comparison to those less socially able, otherwise known as the poor, the disabled, minority groups etc.[1] And so began Eugenics, in which proponents believed that selective breeding would improve the genetic qualities of the human race. If you haven't already thought it, yes it does sound pretty similar to Hitlers Nazi ideology, and for good reason.

Eugenics became an international movement founded on genetics, social theory and policy prescription. And right here in the United Kingdom we were at the forefront, however it soon spread to Germany, France, in fact most European countries, as well as the good old United States. From programs aimed at encouraging those considered "fit" to reproduce, through to marriage prohibition and even the sterilisation of those undesirable types with mental or physical disabilities, and naturally minority groups classed unfit to reproduce. That this seems strikingly similar to the Nazi eugenics program shouldn't surprise you. Indeed, those that attempted to defend themselves at the Nuremberg trials, tried to do so under the justification that Nazi eugenics policy was basically identical to the US programs.[2]

Following the war, the subsequent institution of human rights policies meant a was a gradual decline in the oh so blatent eugenics policies, although some states within the US continued a policy of sterilisation well in to the 1960s. Yet the modern world currently seems tainted by Eugenics, which has recently been amplified by the "send the buggers" back attitude as our nation, (or 52% of them) seemingly attempts to protect the race of "our" island. All this whilst completely ignoring our colonial past. Cries of make Britain great again completely ignores our previous convictions for empire building. Indeed, it is entirely plausible that the Great in Great Britain refers to our occupation of territories such as British India.

As we step out of the European Union (or at least shuffle towards the door having been abandoned by the two rats that conned a nation), it is becoming increasingly clear that the leave vote, was frequently more of a vote to seal up the borders. To protect 'our' national identity, in effect, keep 'them' out, and maintain our (allegedly) superior race. We're losing the empire that we once acquired, colonised or whatever other tag you wish to apply to our imperial reputation. Having plundered our way around the globe, now is the time to batten down the hatches before we suffer the same consequences. At it's height our British Empire consisted of a fifth of the global population and a quarter of all land, we were quite a force to be reckoned with. Yet despite millions of deaths due to famine, brutal detention camps, the massacres of civilians, 44 per cent of a YouGov Poll were proud of our colonial past, even David Cameron thinks it should be celebrated.[3] This blinkered view if our history, coupled with the fear purported by Murdock et al, that another race may do as we did, seems to be driving a huge surge of nationalism around the country. I know, it is good to be proud of your country, just maybe not when you want to block anyone that hasn't popped out of a Vagina in the right part of the globe, or to anyone rich enough. It may seem far fetched, but the Nazi campaign was founded upon Nationalism and Economic downturn...and where are we right now? A hate fuelled rhetoric led by Boris and Nige fuelling far right groups and facing more austerity and cuts for the lower classes. 

So, what is the selection criteria for entry to our imperial island? How do we select whom the superior immigrants are? Do we perform a medical examination? Will it be genetic based? Education? Career prospects? Wealth? Or any other number of methods for selecting who is desirable, whilst avoiding those who may not fit our criteria. Sounding much like the Third Reich yet?

As Bertrand Russell was quoted as saying in 1924; 

‘We may perhaps assume that, if people grow less superstitious, government will acquire the right to sterilise those who are not considered desirable as parents.’

Not the Bertrand Russell quotes that your used to I'd imagine, but it just goes to highlight how accepted eugenics had become.

Whilst our government is currently unable to implement such measures, due to the EU Charter of Fundamental Rights, they are able to do it much more slyly. Take for instance the government’s decision to limit a family’s child tax credits to two children, aimed at dissuading reproduction from those less attractive socio-economic groups. Their is however a clause that allows further payment if the child is the result of a rape (nice bonus touch government). And most of us happily accept this, maybe even nod our head in agreement, "why should we support those who can't afford it", and to some degree you may have a point. Yet it doesn't change the fact that it is a soft way of ensuring those with money can reproduce more easily than those from poor backgrounds

From the other side we are seeing IVF technology advancing to a stage in which we are able to screen for inherited diseases. Sounds great, but calls are afoot for the ability to choose your child right down to the sex or hair colour. Will it be the dystopian social groups that get to avoid the game of chance? The ruling class, those with money, power and elite status will no doubt be able to afford the ability to tinker with procreation. So whilst the elite will be able to ensure that they select preferable genetics, the lower classes will no doubt suffer testing for birth defects [5] and be meekly ushered towards the abortion pamphlets.

As Boris shuffled rather uncomfortably away from Number 10, we must remember that the man he seemed intent on modelling himself on, Sir Winston Churchill (the then Home Secretary), urged the Prime Minister of his day to stop the “multiplication of the unfit”, and we can start to see how close modern policy comes to our haunted past.

​As we snear at those immigrants for "coming over here and taking our benefits" we must turn to Dr Adam Perkins, a lecturer in the neurobiology of personality at King’s College London. Perkins is a social scientist that studies and no doubt holds the image of benefit Britain close to his heart. His academic research (if its possible to call it that) has looked at welfare traits and found that these traits are often inherited through generations, which in his mind helps explain why poverty has a tendency to be passed down from one generation to the next.

His argument rests upon the rise in welfare spending creating a burden upon the rest of us, and by allowing the birth of individuals with inherited laziness, propensity to commit crime, become alcoholics, abuse drugs etc society is further damaged. His remedy is for welfare restrictions to inhibit reproduction, ensuring decent hardworking human stock is allowed to prosper whilst the poor are phased out. Heil.

Perkins work is a complete fantasy, in all honesty he is simply a eugenist, [5] he considers that benefit payments should be restricted until "workless" households lower their birth rates is a Daily Mail dream. Yet his data is sloppy at best, more likely deceptive. His claims that ‘the higher the proportion of unemployed adults in a household, the greater the number of children – on average – it contains', only works if you exclude childless households. I mean I would of won more competitions this year, if you ignore the data from those that I didn't win. If you want to be so bold, you really need to include the full data. The whole thing stinks.

Howwever, that is forgetting one other thing. Genetics research is generally a total crock of %*$@. A $2.7 million crock of %*$@.[6] On that note, we refer to the bastion of knowledge that is Dr. Raymond Peat;

What this is basically saying, (for those who may need to reread Ray's words a few more times for it to sink in) is that life isn't some random genetic game of chance. Your destiny isn't specifically controlled by your genes, rather your genes adapt to your environment and can so do both ways. That your diet and lifestyle effect what happens, eat too much polyunsaturated fatty acids and bingo you may get diabetes. Eradicate the fat and reintroduce sugars, bingo bango, through the magic that is the Randle Cycle you can become undiabetic (a term suggested by one of my clients diabetes nurses, who claimed that he was genetically susceptible to "the diabetes", and that it couldn't be reversed). Do you really have bad genes? Or are they just being fed bad information? Yes we are born with inherited genes, but epiigenetics shows that genes can be turned on and off and that environmental issues such as poor diet, stress etc will affect us. If it were predetermined by our genes, nothing you do would matter. Yet it is evident all around you that people can adapt. We define our genes and shouldn't be defined by them, (unless you subscribe to genetic determinism, then good luck to you), via adequote nutrition, a life purpose, equality, a place in society and by feeling valued, we can effect our outcomes. If someone is forcing our hand through genetic beliefs, social theory and policy prescription this becomes increasingly hard.

So, what does this have to do with our recent EU referendum? Well, EU Charter of Fundamental Rights states;

"(b) the prohibition of eugenic practices, in particular those aiming at the selection of persons;
(c)
the prohibition on making the human body and its parts as such a source of financial gain;
(d)
the prohibition of the reproductive cloning of human beings." [8]

And post-referendum we must ensure these protections stay in place.

While sperm banks boast about screening for everything from autism to red hair [9], and you can pay to select your embryo or its sex. We futher attempt to hold the poor back by means of high education costs (£9000+ for University fees), criminalise those self medicating with drugs, classify them as addicts, restrict welfare despite promoting tax cuts for high earners and corporate welfare, attempt to ban those with different pigmentation or race. The implementation of various nutritional programs (the promotion of polyunsaturated fats, low calorie RDA etc).

For the public, at lot of this has been about race, yet we must remember that the biological differences between us all or practically unmeasurable. Colour cannot be seen by the human eye, it takes the brain to decide what you see.[10] And if that is the case, that means that that ideology about maintaining our imperial whiteness is a learned behaviour. And, much like your genes can adapt both ways, so can you. You can learn that no matter where on the globe someone is born, we are all fundamentally the same. For the race to prosper we need unity and togetherness. Post Brexit I think for the safety of all involved it would be wiser to keep these fundamental rights to life.

References;

1. Sir Francis Galton - https://en.wikipedia.org/wiki/Francis_Galton - en.wikipedia.org/wiki/Francis_Galton

2. Nazi eugenics history - http://historynewsnetwork.org/article/1796​

3. British people are proud of colonialism. http://www.independent.co.uk/news/uk/politics/british-people-are-proud-of-colonialism-and-the-british-empire-poll-finds-a6821206.html
​
4. Birth defects can be diagnosed during pregnancy or after the baby is born, depending on the specific type of birth defect. http://www.cdc.gov/ncbddd/birthdefects/diagnosis.html​x.

5. Mr Perkins’ Welfare Traits http://londoninvestigates.uk/?p=669

6. The failure of the genome https://www.theguardian.com/commentisfree/2011/apr/17/human-genome-genetics-twin-studies

​7. Peat, R. Genes, Carbon Dioxide and Adaptation http://raypeat.com/articles/articles/genes-carbon-dioxide-adaptation.shtml

8. Charter of Fundamental Rights of the European Union - http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX%3A12012P%2FTXT

9. Sperm bank turns down redheads http://www.telegraph.co.uk/news/worldnews/europe/denmark/8768598/Sperm-bank-turns-down-redheads.html
​
10. Our brains, not eyes, see colour ​http://thefutureofthings.com/4180-our-brains-not-eyes-see-color/

I am going to go out on a limb and wager that you have arrived at this post hoping for the 8 top tips for burning fat. If you are looking for quick wins – what I call a ‘buy now, pay later’ approach to health, then you are probably better off redirecting your browser to menshealth.com, getshredded.net, or whatever sites are perpetuating the idea that burning fat is the best way to get lean. 
 
Back in the day, (I'm talking the late 90's) I first stumbled upon a dreadmill under the guidance of a gym instructor called Andy. After a short period of getting to know my new gym programme, I realised it was pretty much the same as every other members. And like the others, I noticed that the results didn't match my expectations. So, I set about my now infamous year of exercise experiment.
 
You may think that I have always been motivated to research and disprove things prior to engaging in them.  You'd be wrong, I came from a sports background, and in the land of sports you do as everyone has done before you. Whilst riding for Team GB I ate pasta like I was advised, and drank random drinks like a good little athlete. However, when I had a crash and injured my knee (someone crashed into my car), my weight gradually crept up and my knee began to deteriorate rapidly, (at this point I was only in my early 20's) so I did what everyone else does...I joined a gym to get fit. This was the beginning of my now famous n=1 experiments.

N=1 is a single subject experiment in which the lone participant (me in this case) is the sole unit of observation. The two things ideally needed are;

• Randomisation
• Repeated measures.

 
The randomisation came from asking a member at the gym to pull 4 sealed options out of a hat;

1. Cardio
2. Resistance Exercise
3. Cardio first followed by Resistance
4. Resistance first followed by cardio

 
The repeated measures simply came from repeating each option more than once to try and replicate the result.
 
Now let me make this implicitly clear, back in those days I had begun work as an Engineer at Rolls Royce. I approached this in a methodical way and not as a true scientist (although science isn’t as rigorous as it should be these days), so do not take this as gold standard research.
 
Despite criticism of n1 studies (such as you need a large group), I still believe to this day we all should to some degree, utilise n1 self experimentation as a strategy for individualising our own healthcare. As opposed to relying upon an authoritarian doctrine that is aimed at the masses. (1)

I find it very easy to commit to the discipline necessary to ensure as thorough experiment as possible, I can partly thank my ASD for that. In all I spent over a year (every single day, even Christmas day as it was a hotel gym, and such was my commitment to the cause) working through the process to conclude which worked best for me. I spent 4 hours a day at the gym (motivated by the experiment and by the hope that I'd regain my health enough to compete properly again).
 
Admittedly I didn't record it as well as I would if I were to redo it (not a chance in hell), but at the end of the period I was 4lbs lighter overall with little difference between the options in terms of results (in fact no noticeable difference). You could conclude (as the gym instructor tried to tell me), that muscle weighs more than fat, only I wasn't more muscular. You could argue that I was a little less flabby but I was fat (my mum called me chunky).
 
This led to the almost famous (it may not be Paris Hilton status but its been widely discussed in some forums on the net, and I did get known as the 6000 calorie diet man for a short period) n=1 diet experiment. I’ve already blogged about this here The No Diet Diet

Ray Peat Forum

180 Degree

Marks Daily Apple

It’s pretty weird to read about yourself online (I only found the top two today whilst searching for some others that I already knew of) and when reading about the 6k calories a day experiment and some of the comments about it, it makes me really concur with Ray Peat when he talks about the importance of taking things in context. Anyway, I digress (I do a lot of that).
 
So, back to the exercise. I was always curious about those heart rate target zones on treadmills. The guidance on the machines basically stated that low level activity, keeping your heart rate closer to 'normal' was the fat burning zone, and as you progress further away to the higher heart rate zones, you are looking at performance benefits and not fat burning, so probably more for athletes. 
 
Using fat, particularly in a gym was seen as the more desirable option, in fact it was the only option. The vast majority of people going to the gym are there for the specific purpose of burning fat. So why would anyone go there and want to use glucose as fuel?  That there was a vending machine selling energy drinks seemed laughable, seeing as it was the antithesis of what people are in the gym to do...this was a serious business and fat was and is the fuel of choice in most commercial gyms.

However this troubled me from the very beginning, and all my studying up until that point (still relatively little compared to now) showed me that glucose was the body’s preferred fuel for anything more strenuous than rest. Lay in bed and you can use lipolysis, in which fats are broken down to release fatty acids for fuel. (Click this link for a little more detail on which tissues prefer which fuel) During a resting state, 85% of your muscles fuel needs are met by fatty acid catabolism, as you move away from resting state this percentage progressively decreases. I just couldn't understand why why everyone was (and still are) completing such punishing exercise regimes with such a fearsome intensity. Why when it was clear that fat was used as low intensity fuel, did they push themselves so hard? Even the gym machines hinted at this very fact...

The reason is simple (although not entirely sensible).  In our quest for lean, the overriding desire is to deplete yourself of glycogen (stored form of glucose) on the basis that the body will then utilise fat instead. The great uneducated who are busy making a lot of dosh, peddling this science fiction and giving people a fast track to ill health say that this can be achieved even quicker by following a low carb diet, by training before breakfast (fasted training) or by consistently performing hard exercise that depletes glycogen stores. However the trade-off of this is that you will degrade your cellular respiration (especially if you are one of the endurance sports victims, I mean athletes). If you want to be fat burner whilst working in those higher zones (70% upwards) then you are going to need some metabolic adaption. I personally think your best place to burn fat is during the night when your asleep and able to maintain a resting state for a long period.
 
To understand your body and how it works, a little better, I’m going to science for a bit, I’m attempting to keep it relatively simple, but it is a fairly complex topic, for slightly more detail please follow this cellular respiration link.  Bear with me, it will be worth it as you will get to know your body better and in turn will not have to listen to the nonsense being peddled by various body coaches and personal drainers.

Cellular respiration is a three step process of how you generate energy, that very same energy that you'll use whilst training. In fact it happens to be the very same energy you'll use for everything your cells need to do, so its pretty important. Sadly it is ignored by most diet specialists who seem intent on blocking your ability to generate energy properly.

Glycolysis occurs within the cell and can occur with or without Oxygen (O2), meaning it can happen if you are sat down relaxing or doing CrossFit.

​It yields two Adenosine triphosphate (ATP).

The Citric Acid Cycle (or Krebs Cycle) occurs within the inner mitochondrial matrix, and is an aerobic process that can only work in the presence of O2. So if you're sat down relaxing it can still work, but, If you're getting out of breath during the Race for Life then it can't. If you remain able to ventilate well you've just got yourself another two ATP.​

The electron transport chain occurs within the mitochondria and is the most important and final stage of cellular respiration. The two stages were preparing for this part. Here our yield of ATP increases to 34 and yet again, oxygen must be present. So, you can see oxygen seems to be key, and without its presence you get stuck in glycolysis which yields much less ATP (energy).

Glucose and oxygen are both essential and hugely anti-stress, so in an ideal world we need to ensure that our body has easy access to both. These are foundational needs,no point in putting in fancy wallpaper in a house that is crumbling into the ground.  The same is true of your body, you need to get the basics right first before you try and do anything else. 
 
Unfortunately we live in a world where it is hipster to restrict both things in the belief that you can biohack yourself to a better body and life.As such what we commonly see in those that produce energy inefficiently via glycolysis, is an Increase in the blood levels of adrenaline, cortisol, and lactate (aka stress hormones) and issues with sugar and insulin regulation.

These are common issues that I see on a daily basis in those displaying symptoms such as diabetes, obesity, cancer, and general degeneration/ageing. These victims, I mean people, also tend to have a decreased respiratory quotient, which means they exhale less carbon dioxide on either my capnograph or my indirect calorimeter (used to measure resting metabolic rate). Measure any of these against a small child and you'll typically see that ageing and disease (along with obesity) correlates with a switch to using fats (free fatty acids to be exact) for fuel instead of glucose. You also tend to see alterations in body temp and pulse, but we've discussed that many times before and will again in the future – but just for a quick reference, body temperature and pulse tend to decline too.
 
What does all this translate to?  Well, in the absence of oxygen (such as when you go against the clock at CrassFit, or take part in the Race for Life (an ironic name if ever there was one), you push yourself into a hypoxic state (i.e. you starve yourself of O2, effectively strangling your cells) as you pant for breath. This causes a stress state, which your body helpfully responds to with adrenaline (and later cortisol), to assist in the hunt for energy.  The adrenaline liberates free fatty acids and tissue into your blood supply to use as fuel. Hurray, you've now achieved your goal, you're a fat burner.  But quite probably not in the way you want to be.
 
This is because the utilisation of free fatty acids (fat burning) does have some major drawbacks.  Firstly, less carbon dioxide is produced, and as I mentioned earlier, CO2 is a diagnostic measure of resting metabolic rate. So right away the evidence is building that breathless exercise is tanking your metabolism (because it is using fat as a fuel, rather than glucose, the same as when you do ‘low carb’). Sure we've all heard the stories that exercise boosts your metabolism, and yeah it does produce that effect temporarily, but as Dr. Peat once said, a better way to achieve that would be a warm bath. I recognise that this doesn’t make for such an interesting Facebook status but its better for you in the long run. 

Another factor in this temporary increase of ‘buy now, pay later’ metaboism is the previously mentioned increased adrenaline levels which stimulates metabolism via the stress reaction. Do you want to rely on stress to keep your metabolism raised? Believe or not, some people do attempt it. Some people are living with the consequences of doing exactly  – Sarah is a prime example, trashed her body with years of dieting and stress and now has an inflammatory bowel condition, more about that another time.
 
Anyway, back to the CO2. Without it you would really struggle to use glucose and oxygen properly. Think of middle to long distance runners and long distance cyclists, they are a group known for training at altitude, where CO2 concentrations are higher which aids recovery and performance. They're also prone to a little EPO (erythropoietin), but that is a whole different story. Dr. Brown who has been used by Nike athletes, is infamous for diagnosing sub-clinical hypothyroidism in athletes, which is is a funny coincidence seeing that you also need adequate thyroid hormone to produce CO2. (As a side note, it is always worth paying attention to the methods athletes will use to both enhance performance and protect their health, such as Maria Sharapova who was recently caught using a drug called Mildronate/Mildonium, which basically aims to help you maintain cellular respiration, something that you can do yourself if you stop participating in endurance exercise and maintain an adequate supply of energy.

The more you use fatty acids, the more you damage the cell and prevent it from being able to generate energy via the three steps mentioned above. This is again a factor in sport, as it takes time for an endurance athlete to adapt and become proficient in performing using free fatty acids rather than glucose. As such, it usually takes till 30+ before these athletes start peaking. And one of the things they train for, is to increase their lactate threshold (more on lactate/lactic acid another time). 
 
Similarly, in the average dieter/gym user it takes a while to adapt, but given the right environment (limit sugars, limit calories, increase exercise, use unsaturated fats, increase protein intake by way of protein shakes and millions of egg whites) by the time you're an adult then you should be doing a fantastic job of slowing things down and becoming that beast that is the hangry FAT BURNER (by now, Im hoping that you are coming to the realisation that the FB (Fat Burner) promise isn’t all it is cracked up to be!) 

Philip Randle, Peter Garland, Nick Hales, and Eric Newsholme proposed what became known as the Randle Cycle in 1963 (2), in which they proposed that a glucose-fatty acid cycle described the competition for fuel selection, specifically between that of glucose and fatty acids. Randle et al were able to identify that one nutrient was able to inhibit the other (3). In short they identified the biochemical mechanism by which fatty acids inhibits the use of glucose and the route which any number of Instanity, Zumba, CrossFit Wodders and numerous others wish to live their days, in an adapted state in which they assume a higher moral ground whilst living sub-standardly. That the randle cycle provides a highly plausible explanation of diabetes pathophysiology, in which energy metabolism becomes dysfunctional, makes you wonder why any Paleoer that can read would aspire to “fatty acid syndrome”. The inhibition of glucose by fatty acids blocks the cells ability to use glucose, which does look pretty damn similar to the description of diabetes, in which the ability for insulin to enable glucose uptake by muscle is inhibited.

Why though would glucose be spared by the body if it is the preferential fuel? Simple, the act of depriving the cell of glucose, such as in a fasted state (hello all you pre breakfast trainers), activates lipolysis and the inhibition of glucose oxidation provides a glucose-sparing effect that works as an essential survival mechanism for the brain during starvation. Yes thats right...fasted training means nothing more than starving yourself and having to use a survival mechanism to assist.   It’s the physiological equivalent of driving on the spare wheel.
 
You may claim you don't get breathless (and this may well be true, but that could just mean that you’re hyperventilating at rest), and that you don't starve yourself on your high protein, high fat, low carbohydrate diet. Yet exercise and a high fat intake have been shown to inhibit glucose use. The unoxidised glucose is even rerouted to glycogen which correlates nicely with the increase of glycogen evident in the muscles of those suffering both diabetes and starvation ​ (2).

“The antagonism between fat and sugar that Randle described can involve the suppression of sugar oxidation when the concentration of fats in the bloodstream is increased by eating fatty food, or by releasing fats from the tissues by lipolysis, but it can also involve the suppression of fat oxidation by inhibiting the release of fatty acids from the tissues, when a sufficient amount of sugar is eaten.” ~ Dr. Ray Peat 

Woah whoa whoa, so you mean to tell me that there is a way of halting this cell damage by simply eating glucose? (4), and it’s never too late to abandon the "lifestyle" and return to so called "dirty eating" aka being functionally nourished and happy?

The inhibition of lipolysis freaks people out, we have been conditioned to believe that we need to burn fats, by people who are making a living out of not understanding basic biology.  It never made sense to me to force our bodies into any state. From my initial days of study as a PT, restoration of metabolism always seemed logical and safe. Would you force a baby to eat fried bacon and bulletproof coffee, with a side of boiled egg whites, to put it into a fatty acid state? I certainly hope not. 
 
We can never use just one fuel, some tissues will prefer fats and some glucose. And so the best thing to do is to give the body a mix of both and then it has everything available at its disposal.  Simples. 

1. Lillie EO, Patay B, Diamant, Issell B, Topol EJ, & Schork NJ. The n-of-1 clinical trial: the ultimate strategy for individualizing medicine? Per Med. 8(2): 161–173, 2012 

2. Randle PJ, Garland PB, Hales CN, & Newsholme EA. The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1: 785–789, 1963.

3. Randle PJ, Newsholme EA, Garland PB. Regulation of glucose uptake by muscle. 8. Effects of fatty acids, ketone bodies and pyruvate, and of alloxan-diabetes and starvation, on the uptake and metabolic fate of glucose in rat heart and diaphragm muscles. Biochem J 93: 652–665, 1964.

4. Taegtmeyer H, Hems R, Krebs HA. Utilization of energy providing substrates in the isolated working rat heart. Biochem J 186: 701–711, 1980.

​C6H12O6 + 6O2 --> 6 CO2 + 6H2O + 38 ATP may or may not make much sense to you, but the equation is basically cellular respiration.

You may not even know what cellular respiration (CR) is, but that will hopefully become a little clearer. This is a fairly basic post aimed at non science based readers so please take that in to account.

CR is a three step process of how you generate energy, that very same energy that you use whilst training, or indeed resting. It happens to be the very same energy you'll use for everything, so its pretty important. Sadly it is currently ignored by most diet specialists who seem intent on in inhibiting its function. If the full process is allowed to occur, we can generate the most available energy from each molecule of glucose that we consume.
 
1. Glycolysis
Glycolysis occurs in the cytoplasm (the internal sub-structures of the cell) and in total is a 10 step process that converts each molecule of glucose into two pyruvic acid molecules.
 
Importantly this process occurs with or without Oxygen (O2), meaning it is an anaerobic process. Thus it can happen if you're sat down relaxing or doing CrossFit.
 
It yields a miserly two Adenosine triphosphate (ATP) per molecule of glucose, plus two NADH (nicotine adenine dinucleotide, which is a co-enzyme carrier for H+ ions that are liberated as the glucose is oxidised). Pyruvic acid moves into the mitochondria where it is prepared for the next stage of cellular respiration.
 
2. Citric Acid Cycle
The Citric Acid Cycle (or Krebs Cycle) occurs within the inner mitochondrial matrix of the cell, and the acetyl group detaches from co-enzyme A to enter the reaction cycle.
 
This process is aerobic, meaning that it that can only work in the presence of O2. So, if you're sat down relaxing and able to ventilate properly, it can still work (as people age or suffer disease, they do tend to suffer from hypoxia even at rest). If you're getting out of breath during the Race for Life, or mid WOD at CrawsFeet then it can't. If you remain able to breath effectively, thn you've just generated yourself another two ATP per glucose molecule (per 2 acetyl CoA), 6 NADH and 2 FADH2.

Electron Transport Chain - Step Three
The electron transport chain occurs within the mitochondria, and electrons are released from NADH and FADH2 which pass along a series of enzymes releasing energy to fuel. 
 
This is the most important and final stage of cellular respiration. The two stages prior to this were mainly a warm up to the main event, and the electron transport chain is where the real party happens. The majority of your ATP is created in this stage, and critically it also requires O2.
 
During this full process our yield of ATP increases to 34 per glucose molecule. So, you can see oxygen seems to be key, and without its presence you get stuck in glycolysis which yields much less ATP.
​
Somehow, the utilisation of glucose has got a bad rep and the mention of it sends the whole world crazy right now. Equally we aren't keen on oxygen, everything promoted in the mainstream media (and that's where most gym instructors and nutritionists gain their education), is about creating an oxygen debt, depleting glycogen (stored glucose) and burning fat. Hit the gym hard and the sweat is just your body crying. Think about it for a minute though, in reality it is complete Insanity (see what I did there).

The current ideology in the health industry is that through a variety of methods (dieting, exercising etc), one can "burn fat", or turn oneself into a "fat burner". To some degree this is true, but, and it is a big but (no pun intended) every organ is fuelled uniquely. This isn't some weird article about sci-fi diets like blood typing, or the metabolic typing diet, it is a brief explanation about the varying metabolic needs within the body.

Before we go any further it is imperative that you understand that adenosine triphosphate (ATP) is the currency of life, the biological source of energy. Not ad is assumed, calories, carbs, fats or protein.

ATP is generated via oxidation of various metabolic fuels, namely;

• Glucose (that nasty substance that Jamie Oliver and various others currently hate)
• Fatty Acids (fats), that substance they hated in the 80's.
• Amino Acids (proteins), the current darling of the macro-nutrients.

Your Brain
It is beyond doubt that the Brain is the most important organ you have, and glucose is the most important fuel it uses. It can use ketone bodies for fuel, but this happens during prolonged starvation, so it may be a worthwhile point to consider if you are engaged in a diet attempts to utilise ketone bodies or one that leave you with bad breath. Your brain is not able to store fuel, therefore relies upon a consistant supply of glucose (that nasty stuff remember). Your brain is quite gluttonous, and on average consumes around 120g of glucose per day (approx 400+ calories). For your brain to work properly it needs a glucose concentration of around 1mM, ultimately if it drops below that we can expect to see coma and brain death.Whilst fatty acids are not able to be utilised during starvation, the previously mentioned ketone bodies can act as a source if the brain is under a great enough degree of stress (starvation).

Your Heart
Your heart muscle is able to function aerobically and primarily uses fatty acids, but ketone bodies may used if needed.

Your Muscles
Muscle on the other hand is able to utilise glucose, fatty acids or ketone bodies, and it also has the ability to store glycogen, that can then be converted to glucose when energy is needed. As mentioned in the main article, during resting state, 85% of your muscles fuel needs are met by fatty acid catabolism. Which really makes you wonder why so many are draining themselves at the gym trying to burn fat.

Yesterday's headline on the BBC website looked so promising, 'Bubbly drink trial 'to boost cancer therapy', and for a moment I had hope that someone with some sense had made a breakthrough in mainstream science (I'd expect them to lose funding shortly after).The story (you can click the link above for the actual article) states that 'scientists are investigating whether bubbly drinks could boost the success of cancer treatments, after winning a Cancer Research UK award for ideas "outside the box".

And for a minute I thought that's it, carbonated drinks are being researched and Cancer Research are paying for it. My client Kim had told me the news and had pointed out that they were seemingly in agreement with research we've discussed for number of years.

The researchers from both Ulster and Oxford universities state that low oxygen levels in tumours is a key reason why radiotherapy and drugs fail. I'd counter that the hypoxia in the tissue is the reason the cancer is able to grow, not the reason 'treatments' have such poor success. Otto Warburg found that oxygen starved cells cannot utilise oxidative metabolism, and thus have to use lactate fermentation, in the absence of oxygen to generate energy. Of late that has been translated and misrepresented as sugar causes cancer by everyone from Jamie Oliver to the World Health Organisation (WHO), but the very presence of lactate in a cancer metabolism is evidence that the cells are deriving energy without oxygen, so it is a metabolic defect much like diabetes.

My thoughts soon turned the moment I realised that it was funded by Cancer Research. I couldn't comprehend that they were intending to fund carbon dioxide research, surely that wouldn't be profitable or patentable? And then I read further, the plan is to develop a drink that is "rich in oxygen micro-bubbles", aimed at targeting the specific cancer cells. No doubt this drink will come at a high cost and be treated as medicine. In some ways it's great that their is the potential for a less toxic agent to be used. However, my experience tells me that pumping oxygen into a cell that has stopped using isn't really the answer. As Dr. Peat has previously stated "Breathing pure oxygen lowers the oxygen content of tissues; breathing rarefied air, or air with carbon dioxide, oxygenates and energizes the tissues".

I wish them luck but if their has been a metabolic adaption and the individual is stuck in glycolysis, unable to perform the other stages of cellular metabolism, including the inability to produce CO2 as an end product, then it would seem wiser to address those issues rather than attempt to hyperventilate the cells with O2.

As discussed in previous posts, without Carbon dioxide (CO2), you can't use oxygen efficiently. If you're an athlete that wants to increase the oxygenation, go train at altitude, sleep in an altitude tent or any other way you can increase the % of CO2 you breath in. Other methods could be drinking carbonated drinks, bag breathing (like you would in a panic attack), using sodium bicarbonate, ensuring you have enough glucose in your diet (and active thyroid hormone), or even using the drug diamox which helps retain CO2, and is used in those suffering altitude sickness or high blood pressure.

In short, it is great that they've looked outside the box. It's just a shame they're looking out of a box that was supplied by the medical industry, which still has a back to front mechanistic view of biology.

She told me her name was Billy Gene, as she caused a scene
Then every head turned with eyes that dreamed of being the one
Who will dance on the floor in the round

People always told me be careful of what you do
And don't go around breaking peoples' hearts
And mother always told me be careful of who you love
And be careful of what you do 'cause the lie becomes the truth

Billy Gene is not my lover
She's just a girl who claims that I am the one
But the kid is not my son
She says I am the one, but the kid is not my son

For forty days and forty nights
The law was on her side
But who can stand when she's in demand
Her schemes and plans
'Cause we danced on the floor in the round
So take my strong advice, just remember to always think twice

A weak way to begin a post but how many chances will I ever get to write about genes, to be honest quite a lot.

There can be no doubting that the Human Genome Project has caused quite a scene.
Every head turned as they dreamed of this sequence being the one.

Despite huge amounts of criticism and many many years since the human genome was sequenced. Hardly a day goes by without some Daily Mail headline heralding the latest genetic breakthrough in the fight against Alzheimer's, Cancer, and Diabetes, in fact pretty much anything. Despite billions of dollars the genetic research on Heart Disease, Cancer, Alzheimer's etc is so insignificant that it is laughable. Well it would be if it weren't for the deep crisis which looms over science as it meanders out of control down the genetics pathway, desperately searching a reason to say I told you so. Yet more often than not falling dangerously close to being filled away in the Science Fiction section of every town library.

Have a little click on this link, unsurprisingly, everything other than the title is hidden away from view of the public.  

http://www.ncbi.nlm.nih.gov/pubmed/21142536

If you were able to access it fully you'd find that it reported that little correlation exists between obesity, diabetes, and your genes.That it is basically a huge steaming pile of *%@^ that does not warrant neither anymore time nor investment.

I had intended to comment originally on the attempts to harvest human organs in pigs labeled gene editing. However, I thought I'd let the remarkable and much missed Ma-Wan Ho explain why the Human Genome is a total washout in this rather brilliant article she wrote.

http://www.i-sis.org.uk/humangenome.php

"The fallacy of genetic determinism is widely recognized (18). Genuine genetic diseases that can be attributed to single genes constitute less than 2% of all diseases. And more and more geneticists are coming around to the view that even those are subject to so many other genetic and environmental influences that there is simply no such thing as a single-gene condition. For the rest, the association between the condition and the specific genes or genetic markers reduces to tenuous ‘predispositions’ or ‘susceptibility’. 
‘Predipositions’ to cancer for example, conceals the fact that important environmental factors are left out of consideration. These include the hundreds of acknowledged industrial carcinogens polluting our environment. It is well-known that the incidence of cancer increases with industrialization and with the use of pesticides. Women in non-industrialized Asian countries have a much lower incidence of breast cancer than the women living in the industrialized west. However, when Asian women emigrate to Europe and the United States, their incidence of cancer jumps to that of the white European women within a single generation. Similarly, when DDT and other pesticides were phased out in Israel, breast cancer mortality in pre-menopausal women dropped by 30%. The overwhelming causes of ill-health are environmental and social. That is the conclusion of a growing body of research findings. Environmental influences swamp even large genetic differences. 
The genetic determinist approach of the human genome programme is pernicious because it diverts attention and resources away from addressing the real causes of ill-health, while at the same time stigmatizing the victims and fueling eugenic tendencies in society. The health of nations will be infinitely better served by devoting resources to preventing environmental pollution and to phasing out agrochemicals, rather than by identifying all the genes that ‘predispose’ people to ill-health. The UK Royal Society produced a report in July, calling for national and international coordination to deal with the dangers posed to humans and wildlife by endocrine-disrupting chemicals, substances thought to mimic or block natural hormones in amounts too minute to trigger a conventional toxic response (19).
But it is the inherent complexity of the human organism and the lack of a concept of the organism as a coherent whole that will continue to frustrate all attempts at understanding health and disease within the dominant, reductionist framework."

Sugar is evil, that nasty white substance is responsible for everything from obesity to cancer. Sugar is identified as a 'food' source that has no nutritional value, and recent World Health Organisation (WHO) advice is that we reduced it despite the actual evidence being weak. There are even calls from celebrity guru's and evangelist chefs encouraging us to completely eradicate it from our diets. The western world is seemingly on an impossible mission to detox from it, and beat their addiction to the Devils food.

Yet despite all the bad press (and the science fiction from Lustig et al), glucose is essential for life. The much maligned substance is actually one of the most important elements of our diet. Remember though, I'm only suggesting that it forms part of our diet and that it shouldn't be feared, not that you should ingest nothing but sugar.

I have previously covered the topic when I looked at some of the hysteria surrounding Jamie Oliver and his unjust crusade to implement sugar taxation. You can review that here. For this post I thought I'd take a look at some of the so called facts around sugar and compare them to that other substance that is devoid of nutrition...H2O.

• One of the main reasons we are told not to consume sugar is that it is has no nutrients and therefore has no benefit and is not needed. So, how does water compare? Well right away we can see that unless you add something to it (like you also could with sugar) then water is devoid of any nutrients. Yet we are still told to drink set amounts such as 8 glasses or 2 litres per day. One individual who consulted with me was consuming a massive 8 litres per day under the instruction of fairly well known guru. At that amount it caused a host of issues, as may drinking huge amounts of sugared drinks. Equally, avoiding either isn't wise. FYI you can get plenty of water from actual food, unless that is you're living on dried food.
• This neatly brings us to point number two, one which all of you sugar hating' water guzzlers out there will no doubt be screaming. That water is important for a multitude of various bodily functions, which is correct, without water your future doesn't look to bright. However, sugar, in particular glucose is essential. Metabolism is a series of organic reactions in order to produce the energy known as Adenosine Triphosphate (ATP) via the degradation of fuel. Many people seem to be under the illusion that what you eat is what you 'burn', ignoring the very complex processes which encompass the metabolism and its generation of energy. Metabolism itself is often thought of simply as how much you can eat. And it is common to hear people discussing others being lucky due to their high metabolism. Metabolism is the sum total of all the enzymatic reactions that occur within the cells, which has four main functions; Extract energy from organic nutrients, convert nutrients for use as building blocks within the cells, assemble the building blocks into other cellular structures form and degrade the biomolecules that perform special functions within cells. So, the energy utilised by your body is ATP and sugars are preferentially catabolised in order to form ATP. Limit your energy or make your body struggle due to the belief that carbs need to be complex, and you're on the way to the slow metabolism that you fear so much.

• Water helps you to lose weight. Typically people are encouraged to drink water before a meal to ensure they aren't mistaking thirst for hunger. You never hear it the other way round, someone being advised that maybe, just maybe their extreme thirst is malnourishment otherwise known as hunger. Personally I'd suggest that proper cellular metabolism, as in a body fuelled via oxidative metabolism at rest as opposed to fatty acid synthesis is a far wiser way to lose weight.
• It helps endurance athletes fight fatigue. Water is attributed as an essential part activity to prevent dehydration during long workouts. Those in the "know" often talk about drinking water treated with carbohydrates in order to maintain maintain fluid balance. What they mean by treated with carbohydrate is that it has been poisoned with that deadly white stuff, probably along with that other white product that suffered many years of bad press...no not cocaine, thats still acceptable, I meant sodium. I hands down guarantee that sugar will be the more effective than water in the fight against fatigue. While both are supposedly nutrient deficient, sugar is at least packed with vital energy. Combine the two and you have a winning recipe, stick in some coffee and may even taste nice.

The evidence doesn't stack up against sugar and the attempt to link it with obesity or tooth decay. The argument that it is unneeded and devoid of nutrients just isn't backed by science. The only thing it seems guilty of is calories, that thing everyone focused on in the '80's. Consume it as part of a varied diet, don't over indulge much the same as water.

150g of Dark Choc (I used Seed & Bean)

71g of Coconut butter (normal unsalted butter is fine)

5 Large Eggs

1/4 of cup of Cane Sugar plus an extra 3 tablespoons for later in the recipe

1 teaspoon of Vanilla Extract

1/8th teaspoon Sea Salt

Heat the oven to 180 deg C

Lightly butter a large cake tin that has a removable base.

Melt the chocolate and butter in a glass bowl over boiling water then leave to cool slightly.

Seperate the eggs.

Mix the yolks and 1/4 cup of sugar till it thickens then mix in the vanilla and the sea salt.

Slowly mix in the chocolate and butter now it has cooled slightly.

Using an electric mixer (or a hand one if you're feeling energetic), mix the egg whites with 3 tablespoons of sugar till it begins to peak.

Slowly add in the egg whites bit by bit to the chocolate mix and continue to mix until the consistency is equal.

Pour into the cake tin and transfer to the oven. Bake for around 25 mins but check that a knife comes out clean.

Once baked, remove from the oven, run a knife round the edge and remove from the tin.

​Once cooled enjoy a slice with cream, ice cream or whatever takes your fancy.

​We are ever moving towards a totalitarian superstate that exercises power and control over our lives, as envisaged by both George Orwell and Aldus Huxley. Authoritarianism shrouds our society and the transition towards a dystopian world happens from the moment you are born. The recent threat to tax sugar is an attempt to punish behaviors by an authoritarian government with a history of poor health advice. Claims made about sugar in regard to both obesity and health are backed up by what is labeled as weak evidence (i.e. not evidence).

As Orwell stated, “ignorance becomes strength” and via the mainstream media, our educational system, we slip into either learned helplessness in which we feel powerless to oppose, or we become ignorant/oblivious to alternatives. As a political tool controlling dissent and critical thought give power or indeed, authority.

As Huxley suggested, social control and ignorance has been introduced via the methods of pleasure and distraction. A world obsessed with celebrity, happily watching reality shows while eschewing actual reality. Chasing identities sold to us by the media sources that we freely trust without question. Allowing industry to freely show us what commodities are necessary to conform be it in social standing or even in the role of sick patient.

Critical thinking is dead, and if I’m honest I think it is squeezed out of us the moment childhood ends and education begins. From the very moment we dampen the inquisitive nature of our children and begin to focus them on curriculum criteria, we begin to kill the possibility freethinking. Daring to oppose the mainstream (group think) opinion risks being ostracisied from the jobs, educational settings and risks your ability to tick the boxes needed to move forward in society.

By the time we become adults we've often lost the ability to ask "why?". Oppression via distractions, diversions and the illusion the authority needs to be respected. Yet we soak it up and shirk at the thought of being asked to stand on our own two feet, to think for ourself and draw our own conclusions away from the vile contrived opinions of the Daily Mail. From sugar hating right through to the deadly C, we happily read and fall inline with all that we are told without question. Often by the time I meet a client they are swimming in a swimming pool of learned helplessness unable to stop themselves from drowning despite being told the water isn't deep, stand up and you can save yourself. Time and time again I throw out pubmed studies and suggest people confront their physician with their own evidence, to be hit back with "my doctor didn't want to discuss it", or "I don't want to upset them".

From a young age we constantly ask our parents “why?” and at times it can be frustrating to constantly receive the same question to every little thing that pops in their inquisitive minds. However, you’re empowering them more than any education they will ever receive, by simply engaging in the question. Help them look for real answers. Encourage the why, standby them if they challenge authority and above all question everything. For it is a dire state to be in when someone is no longer interested standing up and challenging authority. Do the same yourself,be a kid and question everything. 

​Prior to reading this article please be aware that in no way do I intend to offend anyone who has or wishes to raise money for the various cancer charities, I have the upmost respect for anyone who has dedicated their time and effort to a cause in which they believed would help. The criticism is focused on an industry that continues ‘research’ poor theories whilst avoiding biological evidence that won’t generate profit. Countless money is being wasted on an un-winnable war.  
 
The War on Cancer was intended as an effort to research the biology of cancer with the aim of developing ‘effective’ cancer treatments. President Nixon declared War on Cancer when he signed the National Cancer Act of 1971, yet it is a war which ultimately has no end insight with no real progress by the allies in attacking the so called enemy. Forget about ISIS, the War on Cancer has cost the public dear, both in terms of lost life and wasted financial investment. Just like War’s in far away lands, the only benefits seem currently to be those who can profit from an enduring battle. Yesterday was the Anniversary of the Great War (December 23, 1971), is it time we declared peace, stopped fighting and directed our efforts at a scientific evidence based understanding of cancer metabolism?
 
How much has this war cost us? And what, if anything, has it achieved?
161,823 died of cancer in the UK during 2012 http://www.cancerresearchuk.org/content/cancer-mortality-statistics#heading-Zero and the financial costs were no less startling, estimated at ‘over £15 billion’ per year. http://www.bbc.co.uk/news/health-20222759
 
Year upon year we spend more and more on cancer treatment, we raised £522 million for Cancer Research here in the UK between 2014 and 2015 http://www.cancerresearchuk.org/sites/default/files/annual_report_and_accounts_2014-15.pdf
Sadly, despite their claims that we’re beating cancer sooner, we aren’t.  As Kolata (2009) discussed, the cancer death rate, adjusted for the size and age of the population, has only decreased by 5 percent since the 50’s, and even that is debatable. (Read this article about how industry plays with the figures to both keep us donating and impress upon us that progress is being made in the war http://raypeat.com/articles/articles/cancer-disorder-energy.shtml). Cancer remains a major cause of death, and an unknown attacker despite 40+ years of ‘research’. Currently the war efforts are directed towards the Human Genome Project, which is intended to expose the genetic factors that cause cancer. As ever this is currently unable to progress the frontline battle and our frontline troops face an uncertain future as they raise money for research and keep their fingers crossed that aren’t one of the unlucky ones that gets dragged into a dirty war. For more on the gene mutation theory, have a look at this fantastic article by Ray http://raypeat.com/articles/articles/the-cancer-matrix.shtml
 
I have a confession, to my knowledge I have never donated to a Cancer Charity, other than ones set up directly by families in which I know they money is helping them directly at a very difficult time (either to seek treatment not paid for via the National Health Service or just to maintain their ability to survive during tough times). I have donated many hours to assist those in need (if they wish my advice) and will continue to do so. However, I will not put a penny in the pot if it goes towards junk research, as I stated earlier I totally respect anyone who has engaged in actively trying to help but for me the effort is unjustified from two major points.
 

1. The majority of Cancer research is so poor that it is never going to establish a cure or even prevention. Look at how many years this has been ongoing without any progress. We can fire a bomb that goes directly to an address, we can fire a man into space but when it comes to disease (especially cancer) it is down to luck of the draw. You either get it or you don’t. If you do then it needs killing…burn it, cut it out, chop of the effected area and basically maim the person to eradicate the disease. How long you then survive is down to how serious your treatment was, but a tick goes in the ‘Cancer Survivor” box.
2. Running a race, or indeed anything that causes the inability to work aerobically puts you at risk of developing a Cancer Metabolism.

 
So, should you run the race for life, or is it in fact putting you in the firing line? Lactate is produced during aerobic glycolysis when glucose is broken down and oxidized. During intense exercise (anaerobic glycolysis) when oxygen levels are lower, there is increased production of lactate.
 
‘High rate of glycolysis is a metabolic hallmark of cancer, and anaerobic glycolysis promotes energy production under hypoxia (inadequate oxygen in the tissue). Indeed, lactate is associated with poor clinical outcome in several cancers, and whilst initially considered an indicator of the glycolytic flux, we now know that lactic acid directly contributes to tumor growth and progression.’ (Dhup, Dadhich, Porporato, & Sonveaux. (2012). Cellular respiration refers to the metabolic processes occurring within the cells that convert food into adenosine triphosphate (ATP) and waste products. Large molecules are broken down into smaller molecules that releases the energy that we need. Sugar, fatty acids and amino acids are all utilised and oxidised with oxygen (O2).
 
Aerobic respiration requires that we have O2 available in order that we can generate ATP. Pyruvate enters the mitochondria to be fully oxidized by the Krebs cycle resulting in the ‘so called’ waste product ‘carbon dioxide’ as well as water (H2O). The energy produced then breaks the bonds in Adenosine diphosphate (ADP) adding a third phosphate to form the ATP via the metabolic reaction known as substrate-level phosphorylation. NADH is also oxidized to NAD+, yielding 2.5 ATPs and FADH2 (flavin adenine dinucleotide) yields 1.5 ATPs during oxidative phosphorylation (OXPHOS), which provides most of the ATP produced via cellular respiration.
 
The potential of NADH and FADH2 is converted to more ATP via the electron transport chain in which oxygen is the terminal electron acceptor.  In theory 38 ATP molecules can be produced via cellular respiration (2 via glycolysis, 2 via Krebs cycle, and about 34 via the electron transport system). However, the yield can be lower due to various factors and may be anywhere between 29 to 30 ATP per glucose. Aerobic metabolism is much more efficient than anaerobic metabolism (which yields 2 molecules ATP per 1 molecule glucose).
 
Glycolysis is a pathway that can function both with and without oxygen. As discussed above, aerobic conditions produce pyruvate and anaerobic conditions produces lactate.
 
However, without oxygen pyruvate is not metabolised via cellular respiration and instead undergoes fermentation. Pyruvate is no longer transported into the mitochondria, instead it remains in the cytoplasm and is converted to waste products so that it can be removed from the cell. This works to oxidize the electron carriers allowing them to perform glycolysis and remove the excess pyruvate. Fermentation oxidizes the NADH to NAD+ so it can be re-used in glycolysis, which prevents a build up of NADH in the cytoplasm. This waste product is called lactic acid that occurs due to lactic acid fermentation. When your energy needs exceed your supply (such as when running a charity race), the respiratory chain is no longer able to process the hydrogen atoms that are joined by NADH. NAD+ regenerates when the pairs of hydrogen combine with the pyruvate and form the lactate. When oxygen becomes available again NAD+ attaches to hydrogen from the lactate and forms ATP. The fermentation process is far less efficient and produces only 2 ATP compared to the 29-38 ATP produced during aerobic respiration.
 
Otto Warburg's early work on Cancer Metabolism is often misrepresented (you’ll often see Warburg credited as finding that sugar causes Cancer) yet his main observation was that lactic acid was produced by cancer cells even when adequate oxygen was seemingly present. Over exertion (such as when running) depletes our reserves of glucose and we shift to producing lactic acid, which in turn increases cortisol (stress hormone) and causes you to shift to fat and protein as fuel rather than glucose (hurrah you here the fat burning gym junkies cry). How long you have the ability to run for without shifting to using fat or protein for fuel is an unknown factor, basically you could either run out of glucose stores (unless you have a very large rucksack to carry enough fuel for your required distance) or you may fail to consume enough oxygen. Either way its safe to assume that running any sort of distance puts you at an enhanced risk of fat/protein usage as opposed to the preferred source.
 
Forming lactic acid as a by-product of adapted energy metabolism is normal if one is running. For example, if you’re being chased by an attacker then it is far safer to produce fuel via an emergency mechanism if your either low on glucose or oxygen (such as when you’re losing the ability to breath properly mid chase). Long term its not a biomarker you wish to exhibit. Both Warburg and Albert Szent-Gyorgyi pioneered the understanding of respiratory defects being present in Cancer cases. Indeed Koch showed that the ability to efficiently use oxygen corrected a cancer metabolism.
 
References:
 
Kolata. (2009). In long drive to cure cancer, advances have been elusive. The New York Times, April 24.
 
Dhup., S, Dadhich., R, K, Porporato., P, E, & Sonveaux,. P. (2012). Multiple biological activities of lactic acid in cancer: influences on tumor growth, angiogenesis and metastasis. Curr Pharm Des;18(10):1319-30.)
 
Koch, W.F. (1921). The Survival Factor in Neoplastic and Viral Diseases. The Inter. Oxid. Instit., Priest River, Idaho, 83856.

Endorphins are often referred to as the brain's "feel-good" chemicals. More often than not when I describe the lack of actual benefit from cardiovascular exercise, I'm confronted with the 'but it makes me feel good' stance.

Endorphin's are morphine like chemicals, your body's own stash of opiates that help decrease pain and create feelings of euphoria. A legal drug that is produced within your own body. From an evolutionary perspective it would seem that endorphins role is to allow us to persist despite some stressor.

The pituitary gland releases endorphins in response to stress, and that could be strenuous exercise, emotional stress, pain, and even under nourishment i.e.dieting.
Endorphins work to relieve pain and also induce euphoria, which leads to it playing a role in your brain's reward system. In exercisers this is the well known phenomenon "runner's high," which relates to the highs experienced post exercise, and the serious lows if they can't fit in that run or gym session.

From a clinical perspective these "feel-good" chemicals play a role in addiction to exercise and dieting, in which an individual habitually returns to starvation/fasting protocols despite poor previous results. When they discontinue a diet or can't train the stressor is removed and the endorphins are no longer released, leaving the individual with symptoms such as anxiety, pain, depression, guilt etc. Only when the stressor returns does the exerciser/dieter get their fix of opiate-like chemicals.

Thanks to Emma for this propaganda article ​http://www.msn.com/en-gb/health/nutrition/sugar-how-we-came-to-crave-the-food-that-nobody-needs/ar-BBmM1g5?li=AA51YE&ocid=HPCDHP

For those of you that don't want to click on the link and give the site a payday, I've pasted parts of it below. In short they are once again stating that we don't need sugar when I think you'll find that we do. In fact the brain needs around 120g a day and cannot function without it (aside from during prolonged starvation when it reverts to a survival mechanism...oddly some diets attempt to keep you in this shock/stress state).

It seems as though no other substance occupies so much of the world’s land, for so little benefit to humanity, as sugar. According to the latest data, sugarcane is the world’s third most valuable crop after cereals and rice, and occupies 26,942,686 hectares of land across the globe. I think we've already covered this, sugar does is fairly valuable for humanity, it is what our cells rely upon for energy. 

Its main output – apart from commercial profits – is a global public health crisis, which has been centuries in the making. I'd like to see the evidence for this...oddly I can't find any!
​
The obesity epidemic – along with related diseases including cancer, dementia, heart disease and diabetes – has spread across every nation where sugar-based carbohydrates have come to dominate to the food economy. Again I've yet to see any evidence for these bold claims. Correlation doesn't equals causation, I mean it would be daft for me to point the figure at polyunsaturated fatty acids and state that the increased intake of these oils also correlates fairly well with increases in various disease states.

The rest of the article rants on about the socioeconomic impact of sugar and even it's links to slavery. Nasty old sugar, that essential energy that your brain needs to survive has a shady past.