@secondkelping said:
I've run through all of the b vitamins. I get some mild improvement if I take them, but it normally helps with initial growth but does not lengthen life of the follicles for me.
Hi,
Well seen for B5 supplement because I only get 50 % of the RDA with my usual food, which is rather varied.
Coenzyme A (via vitamin B5) is essential for synthesizing the lipids that make up the skin barrier. A sudden, massive influx of Coenzyme A can alter the composition of sebum and the lipids found on the skin's surface. If the skin is already sensitive—or under stress due to hepatic excretion—this localized biochemical change can trigger an inflammatory skin reaction (such as eczema).
Taking high-dose vitamin B5 reactivates the acetylation pathway (involving Coenzyme A). Think of high-dose B5 as bringing a team of heavy-duty cleaners into a house; they clear out the cupboards at lightning speed. However, if the hallway is narrow and cluttered (implying poor motility or irregular transit), and the outdoor trash bin is already overflowing with histamine, the debris will pile up in the middle of the living room—eventually spilling out through the window (manifesting as eczema).
Well, not everyone struggles with sluggish digestion or skin prone to breakouts. However, in cases of stress or low-grade inflammation (such as osteoarthritis), the interactions between B-group vitamins must be taken into account.
Potential bottleneck with high-dose vitamin B5: In the intestines, vitamin B5 utilizes the same transporter as biotin. A functional biotin deficiency—triggered by high doses of B5—typically manifests as skin issues, most notably dermatitis and eczema.
In cases of repeated stress, chronic elevation of cortisol directly hinders the entry of vitamin B3 into cells by altering their membrane transporters. Consequently, very little B3 is able to enter. In the short term, this is not an issue: the cell relies on the B3 already present intracellularly, which functions in the form of NAD+ (NAD+ NADH). In fact, approximately 95% of the NAD+ converted into NADH is continuously recycled within the cell itself.
However, stress and chronic inflammation rapidly deplete vitamin B6 reserves. This deficiency impairs hepatic glycogenosis (the liver struggles to release glucose stored as glycogen—a process dependent on B6). At night, this inability to maintain blood sugar levels leads to reactive hypoglycemia; the body then secretes adrenaline to compensate, which triggers repeated nighttime awakenings. Simultaneously, this lack of vitamin B6 blocks the recycling of amino acids, resulting in an increase in toxic homocysteine within the bloodstream.
NB1: In the Krebs cycle, the cell requires NAD (B3) and FAD (B2). There is an interaction between B3 and B6. There is also an increased need for sulfur and methyl donors. Sulfur often helps manage salicylate overload, while methyl groups help manage histamine load.
NB2: If you "press the accelerator pedal" (i.e., ramp up metabolic activity), you must account for the interplay between vitamins B1, B2, B3, B5, B6, and B8, as well as magnesium—which is frequently in short supply (350–420 mg required). I increase magnesium intake during periods of stress, but never by anticipating a stressful event. Always afterwards. J.P. Curtay recommends three 300 mg doses of elemental magnesium. I would personally use magnesium bisglycinate powder: 1.25 g per dose.
Figure: Krebs cycle
[image: 1793601336662-cyce-de-krebs.%C3%A9nergie-et-vit-b.jpg]
