How We Lost the Nutritional Wisdom of Our Ancestors – Food Pharmacy

Paul Clayton

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How We Lost the Nutritional Wisdom of Our Ancestors

The mid-Victorian diet combined a potent cocktail of anti-inflammatory micro- and phyto-nutrients with very low levels of pro-inflammatory compounds, in a diet that contained very few processed foods. These eating habits, together with their significantly higher levels of physical activity, made overweight and diabetes rare; creating a lifestyle that protected the Victorians against chronic inflammation and gave them near-immunity to the degenerative diseases that maim and kill so many of us today. 

We squandered the Victorian virtues in the name of progress and easier lives, and are paying a very heavy price for that.

We don’t, however, have to recreate Victorian conditions to radically improve our health. Instead, we must untangle the skein of factors that, taken together, make us so sick.

We have to accentuate the positive, eliminate the negative, and look after Mr (and Mrs) In-Between. It’s a simple question of identifying the things we got wrong, and putting them right. 

This starts with the Omega 3 fatty acids and polyphenols, the 1-3, 1-6 beta glucans and the various prebiotic fibers; and includes vitamins D and E, and the trace element selenium.

Our intake of (1-3), (1-6) beta-glucans has been very significantly reduced, for a range of reasons which include the introduction of the synthetic fungicides circa 1950, micro-filtration in brewing in the 1960’s, and our historically low consumption of bread. The uncontrollable increase in asthma and allergy since 1950 [1,2] is indirect but clear evidence of widespread (1-3), (1-6) beta-glucan depletion [3]. 

Intakes of Omega 3 fatty acids and polyphenols have also declined, although these changes started rather earlier than the decline in (1-3), (1-6) beta-glucans and can be traced back as far as the early 20th century [4]. This is due to a progressive shift from basic to processed foods and to our physically inactive lifestyles, which have reduced our calorific requirements.

It is likely that average levels of ‘vitamin’ D have also fallen. In the 19th century rickets was common in the great cities, where coal smoke darkened the skies for weeks at a time; but according to a survey undertaken by the British Medical Association during the 1880’s, the disease hardly existed in small towns with populations of less than 5000, villages, and in the countryside [5]. Rural Victorians spent far more time out of doors than we do, ensuring a good vitamin D status, and some urban workers did as well. They walked to and from work every day and spent much of their leisure time on outdoor pursuits due to an acute shortage of TV’s, smart phones and i-Pads.

Today we have a major problem with vitamin D.

Data from the U.S.  National  Health  and  Nutrition  Examination  Survey found that a staggering 61% (50.8 million) were depleted in D, and 9% of children were clinically deficient [6]. The situation in Europe is as bad, and rickets is re-appearing in some subgroups of the population in the UK, predominantly in those of African-Caribbean and South Asian origins [7,8]. 

The Victorians consumed large amounts of seafood which provided selenium, and nuts and wholegrain foods which provided vitamin E. The fact that we eat less than the Victorians, together with our preference for processed and often nutritionally-depleted foods and our fear of sunlight, has left many of us substantially depleted in these nutrients [9-11] also, and contributed to our  increasing vulnerability to inflammatory and auto-immune diseases [12-17].

At the same time, in an apparent paradox, our sheer lack of physicality has made it very difficult for us to maintain healthy body weight. At our current and historically low levels of physical activity, the satiety mechanisms that keep animals in the wild lean (and which used to work well in humans too, overweight and obesity were rare among the Victorians) break down. Surrounded by convenience foods and bombarded with messages to consume, many of us eat a few hundred calories too many per day; and this, over time, is enough to create the weight problems that affect so many. Excess adipose tissue is pro-inflammatory unless it is protected with lipophile micro- and phyto-nutrients, as are the high levels of blood glucose in diabetes caused by the interlinked factors of physical inactivity and obesity. 

The decline in anti-inflammatory nutrients and the increase in obesity and diabetes provide two of the elements needed for a perfect inflammatory storm.

The third exacerbating factor, which makes the storm inevitable, is our hugely increased intake of pro-inflammatory toxins. The proliferation of fast food franchises with their rapid, high temperature cooking methods has made a very significant contribution to our public ill health; but so has the modern food processing and manufacturing industry, which uses high temperature technologies such as spray drying to speed up production.

In short, the way we live today conspires in many ways against good health. From a health perspective everything that could go wrong, has gone wrong; and the idea touted by Big Pharma that there are simple pills to cure all of our modern ills, makes little sense. (Although it makes good financial sense for the drug companies.)

There is a good deal of science behind the key anti-inflammatory nutrients, and an overwhelming public health case to adding them as fortificants to the major food items in our diet. However, until our politicians start to take public health more seriously than their expense claims, you would be well advised to take matters into your own hands and add the key anti-inflammatory nutrients to your own diet. 

The same goes for reducing your intake of pro-inflammatory toxins, taking more exercise and maintaining healthy weight and blood sugar.

References

1. Haahtela T, et  al. “Asthma programme in Finland: a community problem needs community solutions”. Thorax 56.10 (2001): 806-814.

2. Mannino DM., et  al. “Surveillance for asthma–United States, 1980-1999”. MMWR  Surveillance  Summaries  51.1  (2002): 1-13.

3. Kirmaz C., et  al. “Effects of glucan treatment on the Th1/Th2 balance in patients with allergic rhinitis: a double-blind placebo-controlled study”. European  Cytokine  Network  16.2 (2005): 128-134.

4. Clayton P and Rowbotham J. “How the mid-Victorians worked, ate and died”. International Journal of Environmental Research and Public Health 6.3 (2009): 1235-1253.

5. Owens I. “Geographical distribution of rickets, acute and sub-acute rheumatism, chorea and urinary calculus in the British Islands”. British Medical Journal 1.1464 (1889): 113-116.

6. Kumar J., et al. “Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001-2004”. Pediatrics124.3 (2009): e362-e370.

7. SACN 2997. “Scientific Advisory Committee on Nutrition ACN Update on vitamin D: position statement by the Scientific Advisory Committee on Nutrition”.

8. Lanham-New SA., et al. “Proceedings of the Rank Forum on Vitamin D”. British Journal of Nutrition 105.1 (2011): 144-156.

9. Fulgoni VL., et   al.  “Foods, fortificants, and supplements: Where do Americans get their nutrients?” Journal of Nutrition 141.10 (2011): 1847-1854.

10. Krebs-Smith SM., et al. “Americans do not meet federal dietary recommendations”. Journal of Nutrition 140.10 (2010): 1832-1838.

11. Troesch B., et al. “Dietary surveys indicate vitamin intakes below recommendations are common in representative Western countries”. Journal of Nutrition 108.4 (2012): 692-698.

12. Landrier J-F., et  al. “Lipophilic Micronutrients and Adipose Tissue Biology”. Nutrients 4.11 (2012): 1622-1649.

13. Duntas LH. “Selenium and Inflammation – underlying anti-inflammatory mechanisms”. Hormone  and  Metabolic  Research 41.6 (2009): 443-447.

14. Rayman MP and Rayman MP. “The argument for increasing selenium intake”. Proceedings  of  the  Nutrition  Society  61.2(2002): 203-215.

15. Singh U., et al. “Vitamin E, oxidative stress, and inflammation”. Annual Review of Nutrition 25 (2005): 151-174.

16. Devaraj S., et  al. “Low vitamin D levels correlate with the proinflammatory state in type 1 diabetic subjects with and without microvascular complications”. American  Journal  of  Clinical Pathology135.3 (2011): 429-433.

17. Khoo AL., et al. “Regulation of cytokine responses by seasonality of vitamin D status in healthy individuals”. Clinical and Experimental Immunology 164.1 (2011): 72-79.

This text was originally published here on Thuesday, October 15, 2019.
This is a guest post. The opinions expressed are the writer’s own.

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