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Re: Sugar Sugar!
Nov 18, 2004

[QUOTE]Although Cordain et al1 make a strong argument for the role of diet in acne, we believe that it is difficult to dissociate environmental factors such as diet from genetic factors in their study. The Aché and Kitavan people live in closely knit communities, and therefore genetic factors may play a role in the relative lack of acne in these populations. Several studies point to an association of genetic factors with acne, including studies that demonstrate variations in the prevalence of acne among ethnic groups and the high degree of concordance of acne in twins.15-19

In fact, [U]numerous studies have failed to demonstrate significant differences in sebum composition between subjects with and without acne,[/U] suggesting that overall sebum production and not sebum composition is more important in the development of acne. During periods of starvation, when total caloric consumption is greatly reduced, sebum production is decreased by about 40%,20-21 which could certainly improve acne. However, this reduction occurred with extreme caloric restriction (<100 calories/d [<418 J/d]), a circumstance that is not practical to apply as a therapy, to say the least. [B]In each of these studies, changes in the quantity and quality of sebum were reversed after a normal diet was resumed. [/B] Biochemical studies clearly demonstrate that the sebaceous gland can make lipids (cholesterol, squalene, triglycerides, wax esters, and cholesterol esters) from a variety of substrates (including acetate, glucose, and fatty acids) that serve to donate 2 carbon fragments.22-23 [B]The starvation studies indicate that a dietary source of substrates is needed to produce sebaceous lipids[/B]. The type of food from which substrates are derived may not be important in overall sebum production.

In summary, as proposed by Cordain et al,1 it remains possible that adolescents in westernized societies [B]may be repeatedly acutely hyperinsulinemic due to their highly glycemic diet. Hyperinsulinemia in turn may initiate an endocrine cascade that affects the sebaceous gland and follicular keratinization and involves IGF, IGF binding protein 3, androgens, and retinoid signaling pathways[/B]. Whether adherence to a diet with a low glycemic load can alter acne in other populations is unknown. [/QUOTE]


Now what I liked is that this author didn't assume to know everything and just toss aside information because it didn't fit 100% with someone else's theory. This was written in 2002 and since then there have been additional studies to further support that:

Insulin Resistance is necessary for growth during Puberty, hence the increase in IGF-1 for all adolescence

Androgens are responsible for the development (with IGF-1) of sebaceous glands and sebum production

IGF-1 is responsible for the stimulation, growth of sebaceous glands, sebum production, skin cell hyperproliferation (overgrowth), and hyperkeritinization (thick skin).

Hyperandrogenism can lead to a variety of factors including acne, hirsutism, rheumatoid arthritis, obesity, seborrhea, heart disease, etc. The question is how many of these disease are actually a result of Hyperinsulinemia [U]induced[/U] Hyperandrogenism (as there are overlapping signs)?

That Insulin Resistance is "asymptomatic" for many many years and if left untreated Diabetes Type II results. Therefore it makes sense that Type II Diabetes wouldn't be present until someone's 30s or 40s, but it is slowly becoming more prevelant in younger generations. Asymptomatic means that you won't show any outward signs of a problem...until it worsens or it's too late. However, [I]acanthosis nigricans[/I] (another skin disorder) is one sign of Insulin Resistance and I'm betting acne is yet another sign they haven't officially declared yet.

Insulin Resistance also leads to the production of higher LDL (bad) cholesterol levels and lower HDL (good) cholesterol levels and this has been found in acne sufferers and acneic twins. In fact acneic twins were found to be deficient in a component that's apart of HDL called Apolipoprotiein A1. Furthermore because LDL is higher that means you have higher trigylcerides and free fatty acids, which have the option to not only produce cholesterol (needed for steriod hormone synthesis, like androgens), but also PGE1 (good) and PGE2 (bad, inflammatory) prostaglandins.

Now, based on the above, sebum alone was discounted as being the only culprit, IGF-1 was discounted as being the only culprit, hyperinsulinemia was discounted as being the only culprit, furthermore, microorganisms were discounted as being the only culprit, & hyperandrogenism has also been discounted as being the only culprit. What's my point? Obviously the reason that these factors are present in several types of related diseases, but doesn't ALWAYS produce the same symptoms, has to do with our genetic makeup. You do not have to have high androgen levels to produce acne, but you DO need to have defective or sensitized androgen receptors of the skin!

So, just because the above is true, it doesn't mean that the foods you consume aren't a huge part of the equation. It's like saying "sugar isn't my enemy because I have Diabetes (type I), it's because I don't produce enough insulin." Riiiight, but if you don't produce enough insulin, it's best if you dont consume a whole lot sugar unless you can supply your body with that insulin...otherwise health complications & death results. Same goes with Insulin Resistance or Type II Diabetes, you must either improve the cells insulin utilization (sensitivity), reduce insulin secretion and/or reduce the foods that promote a higher insulin output. Furthermore, when you look at people that do have the obesity gene, it doesn't mean that they can keep eating foods that have been show to ALSO support the incidence of obesity & associated health problems because it's "genetic", they still need to REDUCE their risk.

In that respect, if anyone noticed, you can't produce sebum without androgens. You can't produce the products of sebum & steriod hormones without fats in your diet (good or bad). You can't induce cell uptake of fats without insulin (& lipoproteins, LDL) anymore than can induce the uptake of glucose without insulin. You can't initiate sebum production & skin cell growth without IGF-1, which is also present as a result of the insulin in your blood stream (to reduce Insulin). Yet insulin has the ability to inhibit IGFBP-3 and SHBG production which are neccessary to bind/inhibit & reduce the presence of IGF-1 and Free Androgens. Therefore, when IGF-1 is present, if long enough or in high enough concentrations, pro-inflammatory cytokines will also be present (to reduce IGF-1). Let's not for get that our bodies have the ability to produce anti-inflammatory (PGE1) or inflammatory prostaglandins (PGE2) based on the foods & nutrients we supply. Thus, if you eat a certain way, you will favor inflammatory prostaglandins, such as archiadonic acid, which the presence of pro-inflammatory cytokines encourage the production of!

Therefore as you can see, while the defect for the [I]formation[/I] of acne is probably in the skin's androgen receptors, if you eat a certain way that [B]favors [/B] the production of the above contributors, knowingly or unknowingly, you are solely or further [U]encouraging[/U] the production of acne.

Believe me I've thought of the solution, permanent inhibition or suppression of (some of) the skin's androgen receptors. Unfortunately gene therapy is a looong way off and if they ever do this, it will probably initally target ALL androgen receptors of the body and that's [B]not[/B] a good thing whatsoever. This is why currently the only effective solutions are topical or oral/internal anti-inflammatories and/or anti-androgens. As these two, [B]inflammatory products & androgens, are responsible for the events that lead to the production of acne[/B]. Therefore until gene therapy has figured it out, our best bet, especially for chronic acne sufferers, are to find solutions to the above, such as (natural or prescription) Anti-inflammatories, Insulin Sensitizers, Glucocorticoids, Antiandrogens, DHT Inhibitors & Anti-inflammatory or Hormone Balancing Diets, as these are currently our strongest & most effective options.

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