I hope I'll survive to tell the end of the story. Suffice it to say, my HDL reached a new low (20 mg/dL) last Saturday, when I got finger-pricked at a street fair in Manhattan. Total was 165, TG=95, but the ratio TC/HDL is way high. I've tracked these for 20 years and my HDL range has been 22-42, but what scared me this time was that only last month, during my annual physical, the reading was 31. I lost 1/3 of my already measly and precious HDL [:o]
The only differences in my intake were connected: I dropped the 3g/d niacin and started on 1.5g/d 99% resv. Now I expected to lose a few mg on account of niacin, but not 11! Plus I hoped resv. to have a counterbalancing influence.
The reason behind my dropping B3 was the same that krillin outlined in June:
Niacinamide counteracts the beneficial effects of resveratrol, as anyone who has been paying attention here knows.
J Biol Chem. 2002 Nov 22;277(47):45099-107. Epub 2002 Sep 23.
Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and human SIRT1.
Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M, Sinclair DA.
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
The Saccharomyces cerevisiae Sir2 protein is an NAD(+)-dependent histone deacetylase that plays a critical role in transcriptional silencing, genome stability, and longevity. A human homologue of Sir2, SIRT1, regulates the activity of the p53 tumor suppressor and inhibits apoptosis. The Sir2 deacetylation reaction generates two products: O-acetyl-ADP-ribose and nicotinamide, a precursor of nicotinic acid and a form of niacin/vitamin B(3). We show here that nicotinamide strongly inhibits yeast silencing, increases rDNA recombination, and shortens replicative life span to that of a sir2 mutant. Nicotinamide abolishes silencing and leads to an eventual delocalization of Sir2 even in G(1)-arrested cells, demonstrating that silent heterochromatin requires continual Sir2 activity. We show that physiological concentrations of nicotinamide noncompetitively inhibit both Sir2 and SIRT1 in vitro. The degree of inhibition by nicotinamide (IC(50) < 50 microm) is equal to or better than the most effective known synthetic inhibitors of this class of proteins. We propose a model whereby nicotinamide inhibits deacetylation by binding to a conserved pocket adjacent to NAD(+), thereby blocking NAD(+) hydrolysis. We discuss the possibility that nicotinamide is a physiologically relevant regulator of Sir2 enzymes.
PMID: 12297502
Looks like I can't win for losing. Can't you not die of cardio in the short run and also hope to live a longer life?
As in all good American stories, this too may have a happy ending (yet to be verified). In researching for things that lower your HDL (to see what I did wrong) I came across this link. The apparent conflict is due to acute vs settled weight loss. I did recently lose a few fast pounds and must have caught the transient effect:
http://www.lipidsonl...striction&dpg=3 Caloric Restriction Acutely Lowers HDL-C Level
• Trials of very-low-calorie diets show that HDL-C levels decrease by 2–12 mg/dL during acute caloric restriction.
• After 12 wks, HDL-C returned to pretreatment range, and this trend was still apparent after 1 year.
• Therefore, benefits of weight-loss programs should not be assessed during acute caloric restriction.
Weight and HDL-C
• Inverse correlation between body weight and HDL-C is consistently observed in both men and women.
• For every 3 kg (7 lb) of weight loss, HDL-C levels increase 1 mg/dL.