“Karen” is a beautiful young woman with a slim athletic figure, superb symmetrical features, and bone structure to die for. But soon after her family came to Canada, her facial skin and upper back began to break out in ferocious acne, leaving unsightly scars where pimples had been squeezed. At school she became tagged with the name “Fungus” and bullied into misery. She had been treated for over a year with the usual combination topical gels, clindamycin-tretinoin and benzoyl peroxide-adapalene before coming to see us. These treatments had little positive effect.
Some of the local youth give our Flawless Skin for Teens program a bit of notoriety, not only for the skin improvement it produces, but also because we persuade them to turn organic vegan, much to the consternation of some parents. Karen’s doctor had heard of it and thought it might help her.
Her case is not unusual. I am writing about it because a couple of readers responding to my short article, Bread Brain on gluten causing disease, noted a new book by Dr William Davis MD entitled Wheat Belly, and how it cites a great deal of the evidence showing the devastating health effects of grains, especially wheat. It’s great that this science is finally getting out to the public.
As the most common grain we eat, wheat is a major villain in acne, not because of the gluten, but because of its high glycemic effects. As I write, more than 85% of teens in North America have acne, and most of them eat breakfast cereals.(1)
This continuing epidemic of skin disease used to be a mystery. When Prof. John Yudkin of London University first linked acne to high glycemic carbohydrates in the Western diet in 1967, he was jeered by many of his colleagues.(2)
Even today most physicians are not taught about it because they still get little training in genomics. So most treatments are still ineffective topical drugs. Unless you are incredibly lucky with your choice of doctor, to get effective treatment for acne you have to see a specialist.
Since the 1988–2003 Human Genome Project provided the world with highly accurate sequences for three billion letters in the human DNA code, science has uncovered the genetic basis of many diseases, including acne. Genomic science today shows that Yudkin was absolutely right. We can now measure the responses of genes to nutrition, and we know exactly what causes almost all cases of acne, and how to fix most of them.(2,3)
To skip the scientific gobbledegook, the vast majority of cases of acne occur simply because of the effects of certain foods on expression of a master gene called TORC1 which then activates a slew of other genes. This wayward group vastly increase fat formation, sebum formation, growth of hair follicles, insulin levels, insulin-like growth factor, testosterone, and inflammation directly in the skin.(4,5) All this happens in both men and women. The skin cannot contain the turmoil, so bursts it out through the surface. Superimposed on the hormonal turmoil of puberty, skin hasn’t got a chance.
All the local bacteria and other nasties found in acne are adventitious, that is, they jump onto all this new food in open pimples and pores, and infect, gobble, defecate, reproduce, and set up house. As long as the food keeps coming, they are pretty well impossible to drive out. Acne colonies live on in many people into their 20s and 30s, especially women.(4)
Nothing you can put on the skin surface can do more than temporarily reduce the infection. Some drugs, such as tretinoin (Retin-A) have an effect in reducing the local expression of TORC1 in the skin, but because the hormonal expression is throughout the body, and continually carried to the skin by the bloodstream, it is like a flea on an elephant. Tretinoin can also cause severe irritation. One natural non irritating alternative that reduces acne is a 2% solution of green tea. It works because it contains epigallocatechin gallate (EGCG) which directly regulates TORC1. (5)
Cleaning the skin daily likely has the biggest effect you can get from the outside. But rupturing the pimples is a sure way to get scars, and only provides more food for the bug colony, so the cleaning has to be gentle. The harsh, anti-bacterial soaps often used, and rubbing with cloths are definitely out. The key is to reduce the expression of TORC1 and its downstream cohorts from the inside. You can do this only by eliminating the offending foods from your diet.
Acne is a TORC1 disease caused by the degraded foods that form the bulk of our supermarket supplies. Worst are high glycemic grains, (most common are wheat and corn) high saturated fat foods, and dairy proteins. Bread, bagels, burgers, candy, cereals, cheese, milk and cookies, are just the sort of diet adopted by Karen’s family when they left a mainly rice and vegetable diet to come to Canada.
Once we convinced her that the acne was coming from her food, she had no trouble switching back to a veggie based diet. There are a few other secrets, including vegan proteins. We recommend and use with all our clients a full vegan meal replacement alternative to make sure you are getting enough protein. To find out more about this shake email us at: teamcolgan1@gmail.com.
Any intelligent person can avoid the acne foods. It’s a great nutritional plan against numerous diseases caused by our food. It was no trouble to Karen. Today her face is clear and vibrant. Her girlfriends ask her how she got such beautiful skin. Perhaps she likes to keep a few things secret. I believe they call it social currency.
1. Melnick B, Dietary intervention in acne. Dermatoendocrinol. 2012 January 1; 4(1): 20–32.
2. Yudkin J. Sugar consumption in acne vulgaris and seborrhoeic dermatitis. Brit. Med.J., 1967, 3, 153-155.
3. Melnik BC, Schmitz G.Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. 2009 Oct;18(10):833-41.
4. Cappel M, Mauger D, Thiboutot D. Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Arch Dermatol. 2005 Mar;141(3):333-8.