Inflammatory markers and Lp(a) levels as cardiovascular risk factors in androgenetic alopecia.

Clin Hemorheol Microcirc. 2014 Dec 23. [Epub ahead of print]
Inflammatory markers and Lp(a) levels as cardiovascular risk factors in androgenetic alopecia.
Vayá A1, Sarnago A1, Ricart JM2, López V2, Martinez M1, Laiz B1.

It is not well-established whether patients with androgenetic alopecia (AGA) show a higher cardiovascular risk and higher prevalence of metabolic syndrome (MS). Therefore, we aimed to analyze the cardiovascular risk and the prevalence of MS by means of a case-control study. We determined lipidic, inflammatory, hormonal and insulin resistance parameters with conventional laboratory methods in 50 male early-onset AGA patients and 50 controls. AGA patients did not show statistical differences for insulin resistance (glucose, insulin, C peptide, HOMA), lipids (total-cholesterol, HDL-cholesterol, tryglicerides) or hormonal parameters (testosterone, free androgen index, sex hormone-binding globulin) P > 0.05, respectively. No differences between groups were observed in prevalence of MS or its components (P > 0.05). AGA patients showed higher levels of fibrinogen, C-reactive protein (CRP) and lipoprotein(a) (Lp(a)) (P = 0.016, P = 0.019 and P = 0.032, respectively). In the unadjusted logistic regression analyses, PCR >4 mg/L, fibrinogen >395 mg/dL and Lp(a) >59 mg/dL increased the risk of AGA, but in the adjusted logistic regression analyses, only PCR >4 mg/L and Lp(a) >59 mg/dL independently increased this risk (OR = 5.83, 95% CI 1.33-25.59 P = 0.020; OR = 3.94 CI 95% 1.08-14.43 P = 0.038). The present study indicates that AGA patients do not show differences in either insulin resistance or prevalence of MS. However, AGA patients show a higher cardiovascular risk characterized by an increase in inflammatory parameters and Lp(a) levels.

This is the first report since the Lancet of 2000 published the association between Lp(a) and AGA.

I always recommend the following for those with elevated Lp(a) levels.

TocoSorb

Avoid partially hydrogenated oils (this advice really applies to everyone).

Increase saturated fat (lowers Lp(a) levels)

Reduce your intake of vegetable oils (corn, soy, canola, etc.)

Take vitamin C

Interesting

However ray peat forum says tocotrienols deplete k2

iuyyighghghgkh wrote:Interesting

However ray peat forum says tocotrienols deplete k2

All fat solubles work together. I haven't seen anything in the medical literature mentioning this.
Not everything in the Ray Peat camp is on solid ground.

Do you not recommend taking d3, k2 or magnesium?

What does vitamin c do for inflammation? This is all so interesting and complicated at the same time. Thanks CS

hiilikeyourbeard wrote:Do you not recommend taking d3, k2 or magnesium?

What does vitamin c do for inflammation? This is all so interesting and complicated at the same time. Thanks CS

Yes, I think D3 is essential (or even better a topical form that is now available), and both K2 and magnesium are important.

I wanted to expand a little on the vitamin E topic. When all 8 isomers of vitamin E are taken (that includes all isomers of both tocopherols and tocotrienols), the body works more correctly. Certainly, there is evidence of a single isolated (or worse), iosolated, synthetic iosomer is used can inhibit another fat soluble vitamin or hinder conversion of K1 into MK-4 (K2).

Hautarzt. 2006 Apr;57(4):291-6.
[Sebaceous glands as transporters of vitamin E].
[Article in German]
Ekanayake-Mudiyanselage S1, Thiele J.

Human sebum is produced by sebaceous glands and reaches the skin surface via secretion through the hair shaft. There is experimental evidence that the sebaceous glands and sebum serve as a transport mechanism taking the lipophilic antioxidant vitamin E from the blood to the skin surface. The highest levels of vitamin E are found in the sebum and in the skin lipid film in sebum-rich areas such as facial skin. Recent studies indicate that daily oral supplementation of moderate doses of alpha-tocopherol for at least 3 weeks leads to significant increases of vitamin E levels in human skin sites with a high density of sebaceous glands, such as the face. Thus, the potential photoprotective and antioxidants effects of oral vitamin E, as well as possibly other antioxidants, are site-dependent. These findings should be considered when designing clinical studies to assess the efficacy of oral antioxidants against oxidative stress in the skin.