Obesity: Debate, Dogma and Harvard Dons

Extract from “The Road Not Taken” By Robert Frost

I shall be telling this with a sigh

Somewhere ages and ages hence:

Two roads diverged in a wood, and I—

I took the one less travelled by,

And that has made all the difference.

Some years ago, I was invited by the President of the University of Auckland to deliver one of the university’s public lectures. I chose the title “Obesity: Down the road less travelled” and I tried to show how some of the conventional wisdom on obesity might be a bit too rigid in that it might chose to ignore some awkward data. My overall feeling was that the lay audience enjoyed the talk but that the public health nutrition experts in the audience were not impressed. They were comfortable in their prevailing paradigm. Throughout my professional career as a Professor of Nutrition, I have found that the excitement in research is not showing yet again, albeit under slightly different conditions (old/ young; fit/sedentary; diet A/B, etc),  that some basic tenet of modern nutritional thinking remains safe and sound. That excitement is to be found in the unexplained, unexpected and unusual finding. In proudly pursuing this vision of science, I have been reproached, ridiculed, slandered and shunned. One learns to have a thick skin. 

I was aware of a spat some years ago between a career researcher at the US CDC and the world-renowned Dons at the Harvard School of Public Health. However, it was only recently that I could read the full account of this very public spat. The CDC researcher in question was Dr Katherine Flegal and in a recent paper entitled “The obesity wars and the education of a researcher: A personal account” she provides a detailed account of how Harvard Dons rushed to the parapets of the print and electronic media to condemn, in no uncertain terms, the work of Dr Flegal (1).  

In 2004, researchers at the US Centre for Disease Control (CDC) published a paper in the Journal of the American Medical Association (JAMA) which examined the main causes of deaths in the US. Tobacco was the primary cause of mortality (435,000) with poor diet second, at 400,000 deaths. The dominant factor associated with poor diet was obesity. The paper attracted significant attention and the then director of the CDC, Julie Gerdering predicted that obesity would soon overtake smoking as the leading cause of death in the US. 

But others within the CDC were of the view that this short paper had some flaws and they set about correcting these. Their paper, led by Dr Katherine Flegal, was vetted internally within the CDC and was published in JAMA in 2005. It showed a relationship between bodyweight and mortality rate which was quite different from the original study and which challenged conventional wisdom. The instant the paper appeared, several professors from the Harvard School of Public Health began what can only be described as an extraordinary tirade of abuse, demonising the author and discrediting the paper. This month, Dr Flegal published a paper in a leading cardiovascular journal, outlining in detail the vicious backlash to her challenging paper.

Flegal’s paper differed from the earlier CDC publication in several respects. She used actual measurements of weight and height as opposed to self-reported data which overestimates height and which underestimates weight. Flegal used three recent datasets which were nationally representative of the US population whilst the earlier paper used only one old nationally representative sample. That earlier paper did not adjust for effects of age, sex, smoking or other factors on mortality. Dr Flegal did. The earlier paper had several calculations errors which were eventually accepted by the authors. 

Flegal’s paper showed that as body mass index (BMI), increased, mortality increased but in a manner quite different to conventional wisdom. That wisdom held that at the level of overweight (BMI 25-30), mortality began to rise. Above 30, it began to soar. Flegal’s data did show that mortality rose as BMI rose but not until a BMI of 30 in young people. In older persons, mortality showed no change across the entire spectrum of BMI. 

One would have imagined that the Harvard dons who were instrumental in constructing this conventional wisdom would have invited Dr Flegal to discuss her paper and to explore how both could move forward in the pursuit of best science. Instead, they hit the media. Journalists were told that Flegal’s study was “really naïve, deeply flawed and seriously misleading”. Flegal points out that Professor Walter Willett, the doyen of these dons, in an interview with NPR quipped: “This study is really a pile of rubbish and no one should waste their time reading it”. Willett raised his concerns directly with the Director of the CDC who stood behind Flegal’s work, and a research fellow at Harvard blogged that the paper had been retracted and the Flegal was demoted. All utterly untrue.

 Within a week of the publication, the Harvard dons hastily organised a special symposium at which expert after expert, mostly from Harvard, slated Flegal’s paper. That same week, Flegal was giving a paper at a symposium at Berkeley. Standing at the door was a young woman handing out sheets of paper  setting out why Flegal’s paper was flawed. The matter reached low levels when, students taking courses at Harvard, tweeted that one of the dons had advised that Dr. Flegal’s scientific analysis shouldn’t be trusted because she was “a little bit plump herself”.  

Flegal responded to these attacks exactly as any scientist should by searching the literature on the topic to see what others had found. She conducted a meta-analysis of all published papers which had examined the relationship between mortality and BMI and had her findings published in JAMA in 2013. Her work examined 141 eligible papers and concluded, as she had before, that rising BMI was associated with all cause mortality. However, she noted again that the strength of that relationship was much weaker than conventional wisdom and, again, showed no association with rising BMI within the “overweight “category. In an interview with the BBC, Professor Willett stated: “This is an even greater pile of rubbish” than the study in 2005 and in a radio interview on NPR he repeated this criticism of the 2013 study and separately noted that “rubbish” was a polite term for what he really wanted to say.

The truth is somewhere out there, be it Flegal’s truth or Willett’s truth. It matters a lot in public health to know where that truth lies. But when science gets closer to policy, be it climate change, vaccination programmes, transport or public heath, then science tends to be simplified into bite size pieces, suitable for policy makers. Shades of grey are out of the question and maybe that is necessary for policy makers. However, unanimity of opinion, as has been said, is fine for religion and politics. It has no place in science which must stick solely to risk assessment and be open to changing advice as new data emerges. The Harvard dons should know better. 

(1)Flegal KM. The obesity wars and the education of a researcher: A personal account. Prog Cardiovasc Dis. 2021 Jul-Aug;67:75-79. doi: 10.1016/j.pcad.2021.06.009. Epub 2021 Jun 15. PMID: 34139265.

Covid calories

The Institute of Fiscal Studies (IFS) in London has published a paper entitled: “The dietary impact of the COVID-19 pandemic.”(1)  They used a household level database that records all food and non-alcoholic beverages purchased in supermarkets by a nationally representative sample. Within that database was sub-set of data on food purchases for out-of-home consumption. These two datasets were combined to yield data on the types of foods purchased and their calorific value. Their statistical methodology goes above the head of this blogger but given the reputation of IFS, I am taking their findings as they stand. Their data were longitudinal so they could provide data for the entire period of the pandemic and relate such data to those of the previous non-pandemic year. The figure below outlines caloric intake in the home over the period of the pandemic.

In the weeks before the pandemic, calorie intake at home was comparable to the same period in 2019. Around 10 weeks later, there is a spike in purchases, probably reflecting stockpiling and panic purchasing. For the ensuing 20 weeks of lockdown, caloric intake at home was well above the comparable 2019 period, estimated at 30% higher. From about week 27 to week 39, restrictions were eased and in home caloric intake declined but was still above the comparable levels for 2019. Thereafter, as restrictions were re-introduced, in-home caloric intake began to rise again and at a rapid pace. The figure below shows the composition of the foods purchased. The purchase of fruits, vegetables and snacks remained fairly constant. There was a significant decline in ready-to-eat foods and a sharp rise in the purchase of ingredients, indicating a swing to home cooking. 

There was a significant drop in food expenditure for dine-in restaurants and a significant rise in the purchase of takeaway foods. When in-home and out-of-home data is combined, net caloric intake rose. To directly quote the authors: “Over the period April to June, the impact of the pandemic on total calories was due to households increasing their at-home calories by more than the fall in their out-of-home calories.”

The next set of figures show how out-of-home purchases and calories changed

during the pandemic. 

There was a significant drop in food expenditure for dine-in restaurants and a significant rise in the purchase of takeaway foods. When in-home and out-of-home data is combined, net caloric intake rose. To directly quote the authors: “Over the period April to June, the impact of the pandemic on total calories was due to households increasing their at-home calories by more than the fall in their out-of-home calories.” Finally, the authors examine how household composition influenced the net caloric increase in the pandemic:

Retirees showed the least change in caloric intake relative to 2019 with a graded extent of net caloric gain as household moved from those with low skilled employees (about 10%), through semi-skilled about (15%) and peaking with the highly skilled with an average rise of caloric intakes of 25%. (These calculations are my rough estimates from the above graph). There are ample studies showing that periods of lockdown were associated with weight gain. For example, a 3-month showed very significant weight gain during lockdown : “During the lockdown period, greater pro-portion of women gained weight compared to men (46.1% vs 40.6%, P < .01). The obesity rate after the lockdown increased among women (40.7%-41.7, P < .01) but decreased among men (39.6%-38.6, P < .01) compared to before the lockdown”. The problem with weight gain is that it always unintentional and if left unattended the weight gain will persist. There are lessons to be learned about food habits in lockdown and this paper makes a very important contribution to this area.

 

(1)  https://ifs.org.uk/publications/15503

(2)  Mulugeta W, Desalegn H, Solomon S. Impact of the COVID-19 pandemic lockdown on weight status and factors associated with weight gain among adults in Massachusetts. Clin Obes. 2021 Aug;11(4):e12453. doi: 10.1111/cob.12453. Epub 2021 Apr 14. 

Birth cohorts and obesity: What do they tell us

Every so many years, national data are gathered on dietary habits and such surveys also provide data on many non-dietary variables, including BMI.  The data thus gathered on weight and height refer only to the date of measurement. It cannot tell us when an individual might have become overweight or obese, given that the sample will be comprised of individuals ranging in age from tens to the nineties. Thus, if a sample is taken in 1960, the extent to which subjects watched TV would vary very considerably. However, if a birth cohort born in 1960 is followed thereafter, then they all experience the same opportunity for TV viewing. 

A recent paper in the Proceedings of the National Academy of Sciences, provides data on birth cohorts and obesity in the US(1). They used data from NIH longitudinal studies: The National Longitudinal Study of Adolescent to Adult Health (Add Health) (2); The Americans' Changing Lives (ACL) survey (3); Mid Life in the United States (4); Health and Retirement Study (5). The main aim of the study was to determine for different birth cohorts, the age at which the mean body mass index (BMI) reached 30, indicative of obesity.  The data are presented in the table below:

Birth cohort                             Age in years at

                                             which mean cohort BMI

                                        is equal or greater than 30 kg/m2

1980-1984                              30-39

1965-1969                              40-49

1955-1959                              50-59

1950-1954                              60-69

These data clearly indicate younger cohorts will endure the adverse effects of obesity for decades longer than their older or siblings or their parents. Cohorts born between 1905 and 1945 never reached a mean BMI indicative of obesity throughout their lives. However, all readily hit the overweight range (BMI 25.0-29.9 kg/m2) from their thirties onwards and some of the cohorts were knocking on the door of obesity. For example, the cohort born between 1940-1945 reached a mean BMI of 29.4 in their seventies. 

The data we obtain from birth cohorts are critically important in understanding the epidemiology of obesity. However, many take the uncomplicated but incorrect view that both overweight and obesity are entirely a recent phenomenon. In my book “Ever seen a fat fox – the biology of human obesity” I cover several earlier birth cohort studies and BMI (6) .

Researchers at the US National Bureau of Economic Research examined the birth cohort changes in BMI using data collected by the National Center for Health Statistics covering subjects born between 1882 and 1986 (7). Their results show that in 1880, average BMI was within the normal weight range (20-25 kg/m2) at about 22. Mean BMI of black females reached 25 by 1900, while for white males, black males and white females the dates that a mean BMI of 25 was achieved was respectively, 1905, 1915 and 1920. Again, black females led the way in achieving a BMI in excess of 30 by the year 1940 with all others achieving this about 1960. Another set of research from the same US Bureau provides data on the BMI of US military recruits from 1864 to 1991(8). These are more robust data because they are based not on models but on measured weight and height. If we take men aged 45 years, the average BMI increased from 23.3 to 26.5 over this time period but the greatest part of this increase (60%) was in the period 1894 to 1961. Only 20% of the rise in BMI was explained post 1961. 

We can also look at more modern data gathered in Denmark and which looks at the rate of change in body weight in two groups (9). The first are 19-year-old military recruits studied since 1945. The second is a set of children aged 7,8,9,10 and 11, all born in 1930. In both cases, the prevalence of obesity was low at the outset of the studies at about 3 obese persons per thousand of the population. That trebled by 1960 but remarkably, it did not change at all between 1960 and 1990. However thereafter obesity again trebled to a level of about 30-40 obese persons per 1000 of the population. This wave-like growth in obesity, which I call the tsunami of lard, has also been recorded by the researchers at the US Bureau of Economic Research in their 1882-1991 modeling of the growth of obesity in the US. The concept that the rise in obesity has not been linear but wave-like is important in evaluating the present crisis of obesity. As ever in science, progress in our knowledge grows from embracing anomalies and exceptions and not from burying awkward data. 

(1) Yang YC, Walsh CE, Johnson MP, Belsky DW, Reason M, Curran P, Aiello AE, Chanti-Ketterl M, Harris KM. Life-course trajectories of body mass index from adolescence to old age: Racial and educational disparities. Proc Natl Acad Sci U S A. 2021 Apr 27;118(17): e2020167118. doi: 10.1073/pnas.2020167118. PMID: 33875595.

(2) https://addhealth.cpc.unc.edu/ 

(3) https://www.icpsr.umich.edu/web/NACDA/studies/4690 

(4) http://midus.wisc.edu/puboverview.php 

(5) https://hrs.isr.umich.edu/about

(6) https://www.amazon.com/Ever-Seen-Fat-Fox-Explored/dp/1910820083 

(7) Komlos J, Brabec M (2010) The trend of mean BMI values of US adults, birth cohorts 1882-1986 indicates that the obesity epidemi

began earlier than hitherto thought. National Bureau of Economic Research. Available from:  http://www.nber.org/papers/w15862 .

(8) Costa D, Steckel RH. Long term trends in health. Welfare and economic growth in the United States.  In RH Steckle and R,Floud eds Health and Welfare during Industrialization, Chicago: university of Chicago Press, 1997.

(9) Olsen LW, Baker JL. Holst C, Sørensen TI. Birth cohort effect on the obesity epidemic in Denmark Epid 2006;17:292-295.

Obesity goes viral - but not with Covid

 

It is a given that as soon as a child starts to attend a pre-school creche, they will come home with sniffles and occasionally a sore eye from conjunctivitis. The root cause is an adenovirus which will be readily spread as droplets in expired air and, because the adenovirus is not easily disinfected, it is readily spread by shared surfaces. Sound familiar? There is one particular adenovirus that attracts the attention of those in the obesity field that are capable of thinking outside the box, a rare breed, let it be said. Back in 1982, veterinary researchers in Mumbai noted that when chickens were injected with canine distemper virus, they became very fat. Shortly afterwards, other viruses were shown to be drivers of obesity such as the virus that causes scrapie in sheep or an avian adenovirus known as SMAM-1 . Studies then turned to humans to explore if there might be  link between excess body weight and some virus and the candidate virus that has emerged is the adenovirus 36 or Adv 36. The first study (n= 502) to show this was in 2002, with an infection prevalence of 11% in those of normal weight and 30% among the obese population . Since then, an additional 36 studies have examined the role of  Adv 36 in human obesity and a recent systematic review of the literature in this field  has concluded that: ”Strong evidence suggested a possible association between viral infection and obesity” . In general, this blogger dislikes association studies but in this instance, it is the best we can do since it would be unethical to experimentally infect a human with Adv 36. There are, however,  data other than association data to help us understand the role of Adv 36 in obesity. That very first study of Adv 36 in human obesity also included 26 pairs of twins (20 identical and 6 non-identical). What was important in this study was that infection was discordant among the twins, that is, one twin was positive and one was negative for infectivity. The infected twins had a higher body mass index (26.1 v.24.5 kg/m2) and a higher overall % body fat (29.6 v. 27.5 as measured using hydrondensitometry or dual  emission X-ray absorptiometry).

 

The experimental data from animals consistently shows among chickens, rats and monkeys that experimental infection with Adv 36 causes obesity. All show a significant rise in adiposity and all show no change whatsoever in energy intake. Perhaps the most interesting study was at the Wisconsin Primate Research Centre where blood samples were taken from Rhesus monkeys every 6 months for 90 months. The samples were stored frozen and accessed to test for Adv 36 infection . This study therefore relied on natural infection rather than experimental infection. Only those monkeys that remained  seronegative for Adv 36 over an initial 18 moths were included in the study. During this Adv 36-free period, bodyweight changed very little (0.3% or 0.04 kg). However, once they became naturally infected, body weight increased by 15% or 1.7 kg. 

Both the discordant twin study and the longitudinal monkey study of natural infection provide compelling evidence for a possible role of Adv 36 in human obesity. The stand-out discovery is that neither in experimentally infected or naturally infected animals did energy intake change. So how does Adv 36 cause increased fat mass if it has zero effect on energy intake? It does this by stimulating stem cells in adipose tissue to differentiate into adipocytes thus creating more fat cells (hyperplasia)  . The virus also causes a shift in biochemical regulation of fat and glucose metabolism such that the fat cells get fatter (hypertrophy). All of this centres around a protein enzyme, AMP kinase, which is a central regulator in intracellular levels of energy stores. 

So where does this leave us? The answer is, unchanged. Genes load the gun but the environment pulls the trigger so while obesity is highly heritable (multiple twin studies,) it is the obesogenic environment that matters: cheap, palatable and energy dense foods and a totally sedentary environment. Nobody would suggest that viral infection is the cause of obesity but it deserves more than its current orphaned role. 

Nutrients, immunity and Covid.

Food manufacturers, food celebs and wannabe diet experts often discuss the immune boosting properties of some food or nutrient. Our immune system is a highly complex and  orchestrated network of mechanisms that help us fend off infections and the entry of unwanted foreign matter into our bodies. So, when the issue of “boosting” the immune system is raised, it is not unreasonable to ask what part of the immune system you expect to be boosted. Do you want those antibodies (A type) that line the exterior of the body such as the gut and lungs to be smarter at keeping foreign bodies out? Do you want to boost the ability of the body to produce circulating antibodies (G type) to foreign matter that have gained entry into the body? Do you want to boost the so-called cytokine storm that wreaks havoc in Covid? Do you want to boost those antibodies (E type) that are involved in allergic reactions?

Many nutrients are involved in different parts of the immune system  and a deficiency can cause a significant impairment of that system . But how do you define deficiency? Firstly, measuring dietary patterns to ascertain micronutrient status is a waste of time. At the level of the individual, such measures are totally unreliable. They may give a broad sweep but they lack the definition needed to allow us make any prediction of biochemical deficiency. Secondly, when micronutrient deficiency is measured in dietary terms, it is against particular dietary reference values, the ones you might see on a packet of breakfast cereal.  With these, we can have cut-off points, below which population intakes of a nutrient would be a cause for concern. Many with intakes below that minimum threshold of dietary intake may show biochemical deficiencies but, such is the variation in human nutrient requirements, that many with intakes below that value will be perfectly healthy. 

Cut-off levels, based on blood biochemical values, can sharpen our expectation that an individual is prone to some nutritional disorder and in such instances, nutritional supplements and dietetic advice will help restore these blood value to normal. As normality is restored, the many biochemical pathways that depend on the nutrient in question will be fully operational. But here lies the hub of the problem. Once normality is reached, further intake of the nutrient will have no effect. The petrol tank of a Jaguar has 50% greater capacity than that of a Fiat Punto. Fitting an additional petrol tank will not make the Punto overtake the Jag. When a biochemical need is met, that’s it. 

So should we routinely use nutritional supplements? If someone is restricting their food intake to manage their weight, it might be wise to use them. Equally, as we get older, our appetite falls as does our ability to absorb vitamin B12, and again, their use may be a good insurance. And there are specific clinical needs for certain vitamin supplements such as folic acid in pregnancy, multi-micronutrients in cystic fibrosis or calcium for low bone density. Routine use of nutritional supplements is perfectly acceptable but with the current pandemic, there has been a plethora of recommendations for supplementary intakes of individual minerals and vitamins.

In the present pandemic,  many immune related nutrients have come to prominence, none more so than vitamin D. Recommending vitamin D supplements to boost the immune system begs the question: Is it possible that the immune system of your target population is actually limited by another immune related micronutrient. If you don’t know that, focusing on one vitamin is pretty foolish. Besides vitamin D, many other micronutrients are involved in protecting us from unwanted visitors. Vitamins A and C are centrally involved in maintain the integrity of outward facing barriers such as the lung, the gut and the skin. Vitamin E, zinc, iron, selenium and copper all play a role in the systemic immune system. Fish oil type fatty acids can play a significant anti-inflammatory role, the opposite to immune boosting. So, focusing on one nutrient doesn’t seem to make sense. 

The case has been made that Vitamin D plays a particularly significant role in Covid. A first point to note is that vitamin D is a fat soluble vitamin which is preferentially stored in fatty tissue. As people become overweight and obese, blood vitamin D levels fall as it is shunted into fatty tissue. Body fat is among the highest drivers of Covid complications. A study published by the UK Biobank showed that whereas those with Covid had lower levels of blood vitamin D than those who were healthy, these differences disappeared when the data were adjusted to take account of confounding factors, of which obesity was the most important. 

A recent randomized clinical trial published in the Journal of the American Medical Association examined the effect of boosting Vitamin D status in Covid patients. One group received a single high oral dose of vitamin D which led to a doubling of their blood vitamin D levels. The control group received a placebo which had not effect on their blood vitamin D levels.  The treatment with vitamin D had no statistically significant effect on in-hospital mortality, admission to intensive care  or requirement for mechanical ventilation. Three recent UK reports from government advisory agencies (the National Institute for Clinical Excellence, the Scientific advisory Committee on Nutrition and Public Health England) concluded that there is presently no evidence to support a specific role for vitamin D in the prevention and treatment of vitamin D .  

Eating a healthy diet with lots of variety of food type and food colour, maintaining a healthy weight and keeping fit don’t make headlines. But they save lives.

Nutrients, immunity and Covid.

Food manufacturers, food celebs and wannabe diet experts often discuss the immune boosting properties of some food or nutrient. Our immune system is a highly complex and  orchestrated network of mechanisms that help us fend off infections and the entry of unwanted foreign matter into our bodies. So, when the issue of “boosting” the immune system is raised, it is not unreasonable to ask what part of the immune system you expect to be boosted. Do you want those antibodies (A type) that line the exterior of the body such as the gut and lungs to be smarter at keeping foreign bodies out? Do you want to boost the ability of the body to produce circulating antibodies (G type) to foreign matter that have gained entry into the body? Do you want to boost the so-called cytokine storm that wreaks havoc in Covid? Do you want to boost those antibodies (E type) that are involved in allergic reactions?

Many nutrients are involved in different parts of the immune system  and a deficiency can cause a significant impairment of that system . But how do you define deficiency? Firstly, measuring dietary patterns to ascertain micronutrient status is a waste of time. At the level of the individual, such measures are totally unreliable. They may give a broad sweep but they lack the definition needed to allow us make any prediction of biochemical deficiency. Secondly, when micronutrient deficiency is measured in dietary terms, it is against particular dietary reference values, the ones you might see on a packet of breakfast cereal.  With these, we can have cut-off points, below which population intakes of a nutrient would be a cause for concern. Many with intakes below that minimum threshold of dietary intake may show biochemical deficiencies but, such is the variation in human nutrient requirements, that many with intakes below that value will be perfectly healthy. 

Cut-off levels, based on blood biochemical values, can sharpen our expectation that an individual is prone to some nutritional disorder and in such instances, nutritional supplements and dietetic advice will help restore these blood value to normal. As normality is restored, the many biochemical pathways that depend on the nutrient in question will be fully operational. But here lies the hub of the problem. Once normality is reached, further intake of the nutrient will have no effect. The petrol tank of a Jaguar has 50% greater capacity than that of a Fiat Punto. Fitting an additional petrol tank will not make the Punto overtake the Jag. When a biochemical need is met, that’s it. 

So should we routinely use nutritional supplements? If someone is restricting their food intake to manage their weight, it might be wise to use them. Equally, as we get older, our appetite falls as does our ability to absorb vitamin B12, and again, their use may be a good insurance. And there are specific clinical needs for certain vitamin supplements such as folic acid in pregnancy, multi-micronutrients in cystic fibrosis or calcium for low bone density. Routine use of nutritional supplements is perfectly acceptable but with the current pandemic, there has been a plethora of recommendations for supplementary intakes of individual minerals and vitamins.

In the present pandemic,  many immune related nutrients have come to prominence, none more so than vitamin D. Recommending vitamin D supplements to boost the immune system begs the question: Is it possible that the immune system of your target population is actually limited by another immune related micronutrient. If you don’t know that, focusing on one vitamin is pretty foolish. Besides vitamin D, many other micronutrients are involved in protecting us from unwanted visitors. Vitamins A and C are centrally involved in maintain the integrity of outward facing barriers such as the lung, the gut and the skin. Vitamin E, zinc, iron, selenium and copper all play a role in the systemic immune system. Fish oil type fatty acids can play a significant anti-inflammatory role, the opposite to immune boosting. So, focusing on one nutrient doesn’t seem to make sense. 

The case has been made that Vitamin D plays a particularly significant role in Covid. A first point to note is that vitamin D is a fat soluble vitamin which is preferentially stored in fatty tissue. As people become overweight and obese, blood vitamin D levels fall as it is shunted into fatty tissue. Body fat is among the highest drivers of Covid complications. A study published by the UK Biobank showed that whereas those with Covid had lower levels of blood vitamin D than those who were healthy, these differences disappeared when the data were adjusted to take account of confounding factors, of which obesity was the most important. 

A recent randomized clinical trial published in the Journal of the American Medical Association examined the effect of boosting Vitamin D status in Covid patients. One group received a single high oral dose of vitamin D which led to a doubling of their blood vitamin D levels. The control group received a placebo which had not effect on their blood vitamin D levels.  The treatment with vitamin D had no statistically significant effect on in-hospital mortality, admission to intensive care  or requirement for mechanical ventilation. Three recent UK reports from government advisory agencies (the National Institute for Clinical Excellence, the Scientific advisory Committee on Nutrition and Public Health England) concluded that there is presently no evidence to support a specific role for vitamin D in the prevention and treatment of vitamin D .  

Eating a healthy diet with lots of variety of food type and food colour, maintaining a healthy weight and keeping fit don’t make headlines. But they save lives.