Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature may not be available in some browsers.
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
burtlancast said:Amazing interview, once again.
Thanks to the forum member.
Dorito Loyalist said:Out of curiosity, what's your background getting into this ***t?
You seem like someone genuinely interested in what Ray Peat offers while having passionate preexisting opinions on your own on the matters he discusses.
narouz said:Peat went on to discuss antioxidants and the brain and age pigment,
but it was confusing to me what he concluded about that control group and the ethyl alcohol's
seeming effectiveness....
Anybody understand that?
burtlancast said:narouz said:Peat went on to discuss antioxidants and the brain and age pigment,
but it was confusing to me what he concluded about that control group and the ethyl alcohol's
seeming effectiveness....
Anybody understand that?
He meant exactly what you wrote; ethyl alcohol is nearly as good an antioxydant as Vit E when it comes to prevent lipid peroxydation and stop the production of lipofuschin . He then surmises there must be many others antioxydants able to achieve the same feat, without naming them.
He then stresses the most important point remains not to consume PUFAS and foods rich in iron, rather than to load up on these antioxydants.
Alcohol-induced depression: involvement of serotonin.
Pietraszek MH, Urano T, Sumioshi K, Serizawa K, Takahashi S, Takada Y, Takada A.
Source
Department of Physiology, Hamamatsu University, School of Medicine, Shizuoka-ken, Japan.
Abstract
We examined tryptophan and serotonin (5-hydroxytryptamine) levels in the blood after consumption of alcohol. Forty-five minutes after drinking, whole blood serotonin concentration was significantly reduced, whereas no changes were observed in tryptophan level. The diurnal rhythm of 5-HT in subjects who the day before had drunk alcohol was quite different from the control group, but very similar to that of patients with depression. The results strongly suggest that the mechanism of depression after alcohol drinking may be related to serotonin.
kiran said:I wonder what else alcohol does. Does it actually increase metabolism similar to fructose?
kiran said:Alcohol reduces blood serotonin. That's probably why people self-medicate by drinking.
I wonder what else alcohol does. Does it actually increase metabolism similar to fructose?
burtlancast said:And i know for a fact people drink alcohol for it's extremely high caloric index; it gives ( temporarly) a tremendous energy boost when you need it for physical and strenous activity.
narouz said:kiran said:Alcohol reduces blood serotonin. That's probably why people self-medicate by drinking.
I wonder what else alcohol does. Does it actually increase metabolism similar to fructose?
This surprises me.
I've heard Peat say that alcohol is estrogenic.
Then again: seems like he refers sometimes to the yeast used to make some alcoholic beverages
as being the estrogenic factors--maybe not the alcohol itself...?
Transient hypoparathyroidism during acute alcohol intoxication.
Laitinen K, Lamberg-Allardt C, Tunninen R, Karonen SL, Tähtelä R, Ylikahri R, Välimäki M.
Source
Research Unit of Alcohol Diseases, University of Helsinki, Finland.
Abstract
BACKGROUND:
Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however.
METHODS:
We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol.
RESULTS:
The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001).
CONCLUSIONS:
Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.
Increased aromatization may be a mechanism for feminization of some male alcoholics, as well as for the reported increases in plasma estrogen levels in postmenopausal women subjected to moderate alcohol consumption.
...
In male rats, chronic heavy alcohol administration (36% of total calories=12-18 g/kg/day) led to increased aromatization of androgen in the liver
The effect of alcohol ingestion on hepatic aromatase activity and plasma steroid hormones in the rat.
Gordon GG, Southren AL, Vittek J, Lieber CS.
Abstract
Chronic alcohol ingestion in the rat resulted in increased hepatic aromatase activity, elevation of plasma estradiol, and a decrease in plasma testosterone levels. Testicular incubation studies indicated that the source of the estrogen was not of gonadal origin but was, most likely, due to increased peripheral conversion. The failure of HCG in vitro to restore testicular secretion of testosterone to normal levels suggested a direct action of alcohol, or a metabolic product, on gonadal secretory processes, as distinct from trophic hormone effects. This study demonstrates that many of the hormonal alterations seen in cirrhosis of the liver in man may be produced directly by alcohol feeding without cirrhotic changes in the rat.