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Grapefruit, Flavonoids, Detoxification, and Estrogen

For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.) -Ray Peat, PhD

Maturitas. 1994 Dec;20(2-3):155-63.
Inhibition of 17 beta-estradiol metabolism by grapefruit juice in ovariectomized women.
Schubert W, Cullberg G, Edgar B, Hedner T.
In an open, randomized, cross-over study the concentrations of 17 beta-estradiol and estrone in serum were measured over 192 hours in 8 ovariectomized women after a single oral dose intake of 2 mg micronized 17 beta-estradiol. The subjects were studied with and without grapefruit juice intake containing the three natural flavonoids, naringenin, quercetin and kaempherol, which are found as glycosides in citrus fruit. These flavonoids interact with the metabolism of drugs such as 17 beta-estradiol and other steroids that are extensively metabolised through the P-450NF (P-450 IIIA4) enzyme or closely related P-450 systems. After administration of grapefruit juice, peak estrone (between 2-6 hours after tablet intake) concentrations increased significantly. The AUC0-48 and AUC0-192 for estrone but not 17 beta-estradiol, resulting from a single administration of micronized 17 beta-estradiol, were significantly altered. Combined measured estrogens (i.e. 17 beta-estradiol and estrone) also increased significantly. The relationship between the AUCs for 17 beta-estradiol and estrone was not altered by juice intake indicating that a metabolic step after estrone, i.e. further A and/or D ring conversion was inhibited. This study demonstrates that grapefruit juice may alter the metabolic degradation of estrogens, and increase the bioavailable amounts of 17 beta-estradiol and its metabolite estrone, presumably by affecting the oxidative degradation of estrogens. This food interaction may be one factor behind the interindividual variability in 17 beta-estradiol, estrone and estriol serum concentrations after exogenous administration of 17 beta-estradiol to patients.

grapefruit Pictures, Images and Photos

Eur J Drug Metab Pharmacokinet. 1995 Jul-Sep;20(3):219-24.
Flavonoids in grapefruit juice inhibit the in vitro hepatic metabolism of 17 beta-estradiol.
Schubert W, Eriksson U, Edgar B, Cullberg G, Hedner T.
Naringenin, quercetin and kaempferol, which may be found in glycoside form in natural compounds such as grapefruit, are potent inhibitors of cytochrome P-450 metabolism. The influence of these flavonoids on the metabolism of 17 beta-estradiol was investigated in a microsome preparation from human liver. The flavonoids were added in concentrations of 10, 50, 100, 250 and 500 mumol/l to the microsome preparation. The metabolism of 17 beta-estradiol was concentration dependently inhibited by all the flavonoids tested. Addition of the flavonoids to the microsome preparation did not influence estrone formation, while a potent inhibition of estriol formation was observed. At the highest concentrations tested of the respective flavonoid, there was approximately 75-85% inhibition of estriol formation. However, naringenin was a less potent inhibitor of 17 beta-estradiol metabolism as compared to quercetin and kaempferol. The most likely mechanism of action of the flavonoids on 17 beta-estradiol metabolism is inhibition of the cytochrome P-450 IIIA4 enzyme, which catalyzes the reversible hydroxylation of 17 beta-estradiol into estrone and further into estriol. These hydroxylation processes represent the predominant steps of the hepatic metabolic conversion of endogenous as well as exogenous 17 beta-estradiol. This interaction would be expected to inhibit the first-pass metabolism of 17 beta-estradiol, and this has recently been demonstrated after oral administration of 17 beta-estradiol to women.

J Pharmacol Exp Ther. 1992 Jun;261(3):1195-9.
Inhibition of dihydropyridine metabolism in rat and human liver microsomes by flavonoids found in grapefruit juice.
Miniscalco A, Lundahl J, Regårdh CG, Edgar B, Eriksson UG.
The effects of naringenin, quercetin and kaempferol, flavonoids found in grapefruit as glycosides, on the metabolism of nifedipine and the enantiomers of felodipine were studied in microsomes from rat and human liver. Flavonoid concentrations of 10, 50 and 100 mumol/l were added to rat liver microsomes. The metabolism of nifedipine, (R)- and (S)-felodipine was inhibited to a similar extent, and the inhibition was dependent on the chemical structure and the concentration of flavonoid. Naringenin had lower inhibitory potency than quercetin and kaempferol. These flavonoids exhibited the same order of inhibitory potency in human liver microsomes. No inhibition of naringenin was found, however, until higher concentrations, 300 and 500 mumol/l, were added. A likely mechanism is inhibition of cytochrome P-450 IIIA4, the isoenzyme that catalyzes the oxidation of the dihydropyridine ring to form the corresponding pharmacologically inactive pyridine metabolite. This is a predominant metabolic step that determines the extent of first-pass extraction of dihydropyridines. Grapefruit juice has been shown recently to increase the p.o. bioavailability of the dihydropyridine calcium antagonists nifedipine and felodipine. The interaction may be explained by an inhibition of the first-pass metabolism by flavonoids in grapefruit juice. Furthermore, the results indicate that the rat may be used for in vivo studies of interactions between flavonoids and dihydropyridines or other drugs that are metabolized by cytochrome P-450 IIIA4.

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By Team FPS – November 8, 2011

Dietary Fiber, Bowel Health, and Cancer

Also see:
Fermentable Carbohydrates, Anxiety, Aggression
Bowel Toxins Accelerate Aging
Protective Bamboo Shoots
Endotoxin-lipoprotein Hypothesis
Endotoxin: Poisoning from the Inside Out
Protection from Endotoxin
The effect of raw carrot on serum lipids and colon function
Protective Cascara Sagrada and Emodin

“One of the factors promoting excess cortisol production is intestinal irritation, causing absorption of endotoxin and serotonin. Fermentable fibers (including pectins and fructooligosaccharides) support the formation of bacterial toxins, and can cause animals to become anxious and aggressive. Fed to horses, some types of fiber increase the amount of serotonin circulating in the blood. Grains, beans, and other seeds contain fermentable fibers that can promote intestinal irritation.” -Ray Peat, PhD

“Many doctors advise constipated patients to drink more water and exercise. While there is some physiological basis for recommending exercise, the advice to drink more water is simply unphysiological. A study in Latin America found no evidence of benefit from either of those recommendations, and recommended the use of fiber in the diet. The right kind of fiber can benefit a variety of bowel problems. However, some types of fiber can exacerbate the problem, and some types (such as oat bran) have been found to increase bowel cancer in animal studies.” -Ray Peat, PhD

Nutrition and cancer. 1998. v. 31 (1)
Dietary lignin, an insoluble fiber, enhanced uterine cancer but did not influence mammary cancer induced by N-methyl-N-nitrosourea in rats.
Previous investigations suggested potential breast cancer-preventive properties of dietary fiber from cabbage. The purpose of the present investigation was to determine whether lignin, a component of cabbage fiber, would protect against mammary carcinogenesis by N-methyl-N-nitroso-urea (MNU) in Sprague-Dawley rats. A six-week study was conducted using diets containing 0.5-5% dietary wood lignin (a readily available, purified source). These diets were well tolerated by the rats, and a carcinogenesis study using 5 mg MNU/100 g body wt iv at 50 days of age was conducted, with the 2.5% lignin diet fed from 6 through 8 weeks of age followed by 5% lignin diet until 20 weeks after MNU. Dietary lignin and MNU treatment increased food consumption (p < 0.05), and body weight was slightly reduced at 10 and 20 weeks after MNU in the MNU-5% lignin diet group (p < 0.05). Serum estradiol was not altered by dietary lignin or MNU treatment, but uterine weights were highest in the MNU-control diet group 4 and 12 weeks after MNU. Expression of creatine kinase B, an estrogen-responsive gene, was lower in the uteri of the MNU-lignin diet group than in other groups at 20 weeks. Mammary carcinogenesis was not altered by dietary lignin. However, uterine endometrial adenocarcinoma was observed only in the MNU-lignin diet group (4 carcinomas/40 effective rats) (p < 0.05).

Nutr Cancer. 1984;6(2):77-85.
Enhancement of 1,2-dimethylhydrazine-induced large bowel tumorigenesis in Balb/c mice by corn, soybean, and wheat brans.
Clapp NK, Henke MA, London JF, Shock TL.
This study was designed to determine the effects of four well-characterized dietary brans on large bowel tumorigenesis induced in mice with 1,2-dimethylhydrazine (DMH). Eight-week-old barrier-derived male Balb/c mice were fed a semisynthetic diet with 20% bran added (either corn, soybean, soft winter wheat, or hard spring wheat) or a no-fiber-added control diet. Half of each group was given DMH (20 mg/kg body weight/week, subcutaneously for 10 weeks) beginning at 11 weeks of age. Surviving mice were killed 40 weeks after the first DMH injection. Tumors were not found in mice not subjected to DMH. In DMH-treated mice, tumors were found almost exclusively in the distal colon. Tumor incidences were as follows: controls, 11%; soybean group, 44%; soft winter wheat group, 48%; hard spring wheat group, 58%; and corn group, 72%. Tumors per tumor-bearing mouse ranged from 1.4 to 1.6, except in the corn group, which had 2.1. A positive correlation was found between percentage of neutral detergent fiber in the brans and tumor incidences but not between the individual components of cellulose, hemicellulose, or lignin. The enhancement of DMH-induced large bowel tumorigenesis by all four bran types may reflect a species and/or mouse strain effect that is bran-source related. These data emphasize the importance of using well-defined bran in all “fiber” studies.

Cancer Res. 1983 Sep;43(9):4057-61.
Enhancement of rat colon carcinogenesis by wheat bran consumption during the stage of 1,2-dimethylhydrazine administration.
Jacobs LR.
These results demonstrate that dietary wheat bran, a fiber which produces a hyperproliferative response in the colon, significantly increases colon carcinogenesis when fed to rats during the stage of carcinogen administration. This effect appears to be further enhanced when the wheat bran is totally removed from the diet following the stage of carcinogen administration. These data indicate that the hyperproliferative effects of wheat bran appear to outweigh any preventive actions that bran may have on colon carcinogenesis by altering the bulk of intestinal contents and their transit time through the bowel.

Proc Soc Exp Biol Med. 1986 Dec;183(3):299-310.
Relationship between dietary fiber and cancer: metabolic, physiologic, and cellular mechanisms.
Jacobs LR.
The relationships between fiber consumption and human cancer rates have been examined, together with an analysis of the effects of individual dietary fibers on the experimental induction of large bowel cancer. The human epidemiology indicates an inverse correlation between high fiber consumption and lower colon cancer rates. Cereal fiber sources show the most consistent negative correlation. However, human case-control studies in general fail to confirm any protective effect due to dietary fiber. Case-control studies indicate that if any source of dietary fiber is possibly antineoplastic then it is probably vegetables. These results may mean that purified fibers alone do not inhibit tumor development, whereas it is likely that some other factors present in vegetables are antineoplastic. Experiments in laboratory animals, using chemical induction of large bowel cancer, have in general shown a protective effect with supplements of poorly fermentable fibers such as wheat bran or cellulose. In contrast, a number of fermentable fiber supplements including pectin, corn bran, oat bran, undegraded carageenan, agar, psyllium, guar gum, and alfalfa have been shown to enhance tumor development. Possible mechanisms by which fibers may inhibit colon tumorigenesis include dilution and adsorption of any carcinogens and/or promoters contained within the intestinal lumen, the modulation of colonic microbial metabolic activity, and biological modification of intestinal epithelial cells. Dietary fibers not only bind carcinogens, bile acids, and other potential toxins but also essential nutrients, such as minerals, which can inhibit the carcinogenic process. Fermentation of fibers within the large bowel results in the production of short chain fatty acids, which in vivo stimulate cell proliferation, while butyrate appears to be antineoplastic in vitro. Evidence suggests that if dietary fibers stimulate cell proliferation during the stage of initiation, then this may lead to tumor enhancement. Fermentation also lowers luminal pH, which in turn modifies colonic microbial metabolic acidity, and is associated with increased epithelial cell proliferation and colon carcinogenesis. Because dietary fibers differ in their physiochemical properties it has been difficult to identify a single mechanism by which fibers modify colon carcinogenesis. Clearly, more metabolic and physiological studies are needed to fully define the mechanisms by which certain fibers inhibit while others enhance experimental colon carcinogenesis.

Prev Med. 1987 Jul;16(4):540-4.
Fiber, stool bulk, and bile acid output: implications for colon cancer risk.
McPherson-Kay R.
Dietary fiber has direct effects on stool bulk and bile acid output that may be of relevance in the etiology of colon cancer. Most types of fiber increase the total volume of stool and reduce the concentration of specific substances, including bile acids, that are in contact with the bowel wall. However, fibers differ in their effect on stool bulk, with wheat fiber being a more effective stool bulking agent than fruit and vegetable fibers. In addition, the extent to which a specific fiber reduces bile acid concentration will be modified by its concomitant effects on total fecal sterol excretion. Whereas wheat bran reduces fecal bile acid concentration, pectin, lignin, and oat bran do not. These three fibers significantly increase total bile acid output. Bile acids act as promoters of colonic tumors in mutagenesis assay systems and in various animal models. Human epidemiological studies show a relationship between various dietary variables, including fat and fiber intake, fecal concentration of bile acids, and colon cancer risk.

Journal of Surgical Oncology Volume 52, Issue 2, pages 77–82, February 1993
The effect of the fiber components cellulose and lignin on experimental colon neoplasia
David A. Sloan MD, David M. Fleiszer MD, Geoffrey K. Richards MB, David Murray MB, Rea A. Brown MD
Sixty Sprague-Dawley rats were pair-fed one of three nutritionally identical diets. One diet contained “low-fiber” (3.8% crude fiber); the others contained “high fiber” (28.7% crude fiber) composed of either cellulose or lignin. Although both “high fiber” diets had similar stool bulking effects, only the cellulose diet was associated with a reduction in 1,2-dimethylhydrazine (DMH)-induced colon neoplasms. The cellulose diet was also associated with distinct changes in the gut bacterial profile and with a lowered serum cholesterol.

Food Chem Toxicol. 1984 Jul;22(7):573-8.
Effect of Metamucil on tumour formation by 1,2-dimethylhydrazine dihydrochloride in mice.
Toth B.
The effect of the plant cellulose metamucil on the tumorigenicity of 1,2-dimethylhydrazine dihydrochloride (1,2-DMH) was studied in random-bred Swiss mice. Three groups of mice, which were 5, 6 and 6 weeks old at the beginning of the experiment, were given the following treatments: (1) metamucil (20%, w/w) in powdered diet for their lifespan; (2) 1,2-DMH, ten weekly subcutaneous injections at 20 mg/kg body weight; (3) combination of treatments given to groups 1 and 2. The administration of metamucil enhanced the appearance of colon tumours induced by 1,2-DMH in males only. Metamucil had no statistically significant effect on the development of tumours elicited by 1,2-DMH at seven additional sites. It was expected that a high amount of dietary fibre would inhibit carcinogenesis in the large intestine. Instead, metamucil increased the incidence of colon tumours induced by 1,2-DMH, although only in males.

J Nutr. 1989 Feb;119(2):235-41.
Independent effects of fiber and protein on colonic luminal ammonia concentration.
Lupton JR, Marchant LJ.
The potential interactive effects of protein and fiber on cecal and colonic surface areas, colonic luminal ammonia concentrations, luminal pH and blood indices of nitrogen metabolism were tested using two levels of protein (8% and 24%) and two types of fiber (8% pectin or cellulose). Pectin supplementation resulted in larger cecal surface areas and longer large intestines than those of rats fed fiber-free or cellulose-supplemented diets. All high protein diets resulted in total large bowel luminal ammonia (NH3 + NH4+) concentrations that were twice as high as their low protein counterparts (P less than 0.05). The effect of fiber on ammonia concentration depended on the fiber type. In the distal colon, pectin-fed animals had three times the ammonia concentration of the fiber-free animals, and 4-5 times the ammonia concentration of the cellulose-fed animals (P less than 0.001). Blood urea nitrogen values were higher in the high protein than in the low protein groups (P less than 0.05), and highest in the high protein/pectin animals (P less than 0.01). This study clearly demonstrates that luminal ammonia concentration is dependent upon both protein level and fiber type, and that a fermentable fiber (pectin), rather than decreasing colonic ammonia concentrations, actually increases them several-fold.

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By Team FPS – November 5, 2011

Estrogen, Serotonin, and Aggression

Also see:
Fermentable Carbohydrates, Anxiety, Aggression
Anti Serotonin, Pro Libido
Gelatin > Whey
Thyroid peroxidase activity is inhibited by amino acids
Whey, Tryptophan, & Serotonin
Tryptophan, Fatigue, Training, and Performance
Carbohydrate Lowers Free Tryptophan
Protective Glycine
Intestinal Serotonin and Bone Loss
Hypothyroidism and Serotonin
Estrogen Increases Serotonin
Gelatin, Glycine, and Metabolism
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Intestinal Serotonin and Bone Loss

“Estrogen is often said to achieve some of its “wonderful” effects by increasing the effects of serotonin…Many experiments have shown that estrogen is very important for aggressive behavior in animals, and estrogen promotes serotonin’s actions. Some research shows that increased serotonin is associated with certain types of increased aggressiveness, and antiserotonin agents decrease aggresiveness (Ieni, et al., 1985; McMillen, et al., 1987)…” -Ray Peat, PhD

“…there is clear evidence from both animal and human studies that serotonin, like estrogen, is associated with aggression, but the dominating stereotype is that serotonin is the agent of serenity and peace.” -Ray Peat, PhD

Horm Behav. 2006 Aug;50(2):338-45. Epub 2006 Jun 6.
Individual differences in estrogen receptor alpha in select brain nuclei are associated with individual differences in aggression.
Trainor BC, Greiwe KM, Nelson RJ.
“When males were treated with fadrozole (an aromatase inhibitor), aggressive behavior was reduced, although castration did not reduce aggression. These results suggest that estrogens modulate aggressive behavior by acting on a circuit that includes the LS, vBNST, and AHA and that the source of estrogens is non-gonadal. Fadrozole also decreased c-fos expression in the lateral septum following aggressive encounters. Although the effects of estrogen on aggression appear to involve regulation of neuronal activity in the LS, additional processes are likely involved. These results suggest that estrogen acts in a specific subset of a complex network of nuclei to affect aggressive behavior.”

Front Neuroendocrinol. 2006 Jul;27(2):170-9. Epub 2006 Jan 10.
Estrogenic encounters: how interactions between aromatase and the environment modulate aggression.
Trainor BC, Kyomen HH, Marler CA.
“Thus, differences in aromatase enzyme activity, estrogen receptor expression, and related cofactors may have important effects on how steroids affect aggressive behavior. Hormone manipulation studies conducted in a wide variety of species indicate that estrogens modulate aggression. There is also growing evidence that social experience has important effects on the production of estrogen within the brain, and some cases can not be explained by androgenic regulation of aromatase. Such changes in central aromatase activity may play an important role in determining how social experiences affect the probability of whether an individual engages in aggressive behavior. Although studies have been conducted in many taxa, there has been relatively little integration between literatures examining aggression in different species. In this review, we compare and contrast studies examining aggression in birds, mammals, and humans. By taking an integrative approach to our review, we consider mechanisms that could explain species differences in how estrogen modulates aggression.”

Hormones and Behavior 53 (2008) 192–199
Rapid effects of estradiol on male aggression depend on photo period in
reproductively non-responsive mice
BrianC. Trainor M. Sima Finy, Randy J. Nelson
“However, males housed in short days were significantly more aggressive than males housed in long days. Similar to previous work in beach mice (Peromyscus polionotus), estradiol rapidly increased aggression when male California mice were housed in short days but not when housed in long days. These data suggest that the effects of photoperiod on aggression and estrogen signaling are independent of reproductive responses. The rapid action of estradiol on aggression in short-day mice also suggests that nongenomic mechanisms mediate the effects of estrogens in short days.”

Proc Natl Acad Sci U S A. 2007 Jun 5;104(23):9840-5. Epub 2007 May 24.
Photoperiod reverses the effects of estrogens on male aggression via genomic and nongenomic pathways.
Trainor BC, Lin S, Finy MS, Rowland MR, Nelson RJ.
We demonstrate that the behavioral effects of estrogens on aggression are completely reversed by a discrete environmental signal, day length. Selective activation of either estrogen receptor alpha or beta decreases aggression in long days and increases aggression in short days. In the bed nucleus of the stria terminalis, one of several nuclei in a neural circuit that controls aggression, estrogen-dependent gene expression is increased in long days but not in short days, suggesting that estrogens decrease aggression by driving estrogen-dependent gene expression. Estradiol injections increased aggression within 15 min in short days but not in long days, suggesting that estrogens increase aggression in short days primarily via nongenomic pathways. These data demonstrate that the environment can dictate how hormones affect a complex behavior by altering the molecular pathways targeted by steroid receptors.

The Ohio State University. Department of Psychology Honors Theses; 2006
Effects of Estrogen on Aggressive Behavior
Nelson, Randy
Estrogens are known modulators of aggression however, the specific action of estrogens on brain function has not been determined. In a correlational study, the number of estrogen receptors in regions of the hypothalamus and limbic system was correlated with aggressive behavior in a domestic strain of mice (CD-1). To determine whether these correlations reflect the effect of estrogen on aggression, the production of estrogen was manipulated by an aromatase inhibitor (fadrozole) to observe the subsequent effects on aggressive behavior. Reduction of estrogen production resulted in a decrease in aggressive behavior, suggesting that estrogen acts to increase aggression.

Serotonin

Naunyn Schmiedebergs Arch Pharmacol. 1987 Apr;335(4):454-64.
Effects of gepirone, an aryl-piperazine anxiolytic drug, on aggressive behavior and brain monoaminergic neurotransmission.
McMillen BA, Scott SM, Williams HL, Sanghera MK.
In support of this conclusion was the observed potentiation of antiaggressive effects by blocking 5HT receptors wit small doses of methiothepin or methysergide, which would exacerbate the decreased release of 5HT caused by gepirone. These results are in harmony with reports that decreased serotonergic activity has anxiolytic-like effects in animal models of anxiety.

Eur J Pharmacol. 1985 May 8;111(2):211-20.
Maternal aggression in mice: effects of treatments with PCPA, 5-HTP and 5-HT receptor antagonists.
Ieni JR, Thurmond JB.
Drug treatments which influence brain serotonergic systems were administered to lactating female mice during the early postpartum period, and their effects on aggressive behavior, locomotor activity and brain monoamines were examined. P-chlorophenylalanine (200 and 400 mg/kg) and 5-hydroxytryptophan (100 mg/kg) inhibited fighting behavior of postpartum mice toward unfamiliar male intruder mice. These drug-treated postpartum females showed increased latencies to attack male intruders and also reduced frequencies of attack. In addition, postpartum mice treated with the serotonin receptor antagonists, mianserin (2 and 4 mg/kg), methysergide (4 mg/kg) and methiothepin (0.25 and 0.5 mg/kg), displayed significantly less aggressive behavior than control mice, as measured by reduced number of attacks. Whole brain monoamine and monoamine metabolite levels were measured after drug treatments. The behavioral results are discussed in terms of drug-induced changes in brain chemistry and indicate a possible role for serotonin in the mediation of maternal aggressive behavior of mice.

Pharmacol Biochem Behav. 1976 Jul;5(1):55-61.
The role of serotonergic pathways in isolation-induced aggression in mice.
Malick JB, Barnett A.
Male mice that became aggressive following four weeks of social isolation were treated with seven known serotonin receptor antagonists. All of the antiserotonergic drugs selectively antagonized the fighting behavior of the isolated mice; the antiaggressive activity was selective since, at antifighting doses, none of the drugs either significantly altered spontaneous motor activity or impaired inclined-screen performance. Antagonism of 5-HTP-induced head-twitch was used as an in vivo measure of antiserotonergic activity and a statistically significant correlation existed between potency as an antiserotonergic and potency as an antiaggressive. PCPA, a serotonin depletor, also significantly antagonized isolation-induced aggression for at least 24 hr postdrug administration.

Pol J Pharmacol Pharm. 1979 Mar-Apr;31(2):97-106.
Determination of the role of serotonergic and cholinergic systems in apomorphine–induced aggressiveness in rats.
Roliński Z, Herbut M.
Aggressive behavior was produced in rats by administration of apomorphine (APO) 20 mg/kg ip. Serotonin (5-HT) agonists, L-tryptophan or 5-hydroxytryptophan and a MAO inhibitor, pargyline, suppressed the APO-induced aggressiveness. However, cyproheptadine was the only one of four 5-HT antagonists used which potentiated the aggressive behavior.

Animal studies show that darkness stimulates both aggression and eating (Russell and Singer, 1983), and that serotonin increases, while antiserotonin drugs decrease, aggression (Carlini and Lindsey, 1983). -Ray Peat, PhD

Physiol Behav. 1983 Jan;30(1):23-7.
Relations between muricide, circadian rhythm and consummatory behavior.
Russell JW, Singer G.
Three forms of behavior–muricide, eating, and drinking–have been studied at six photic periods during a 12/12 hr light/dark circadian cycle to which the subjects have been habituated. One hundred and eight rats served as subjects, 18 per photic period. The frequency of muricide was recorded for each period and subsequent food and water intakes were measured during a 1 hr test period. Results show a significantly higher frequency of muricide during the dark than during periods of light. Food intake covaried significantly with the incidence of muricide rs = 0.89, p less than 0.05), while no such relationship was found between muricide and water intake (rs = 0.17, p less than 0.05). The findings are consistent with reports of circadian changes in other rodent behaviors, including rhythmicity in home-cage and in shock-induced aggression. Covariation of muricide and eating does not establish a causal relation between the two. Three models of physiological mechanisms which might provide substrates for the covariance are discussed.

Braz J Med Biol Res. 1982 Oct;15(4-5):281-3.
Effect of serotonergic drugs on the aggressiveness induced by delta 9-tetrahydrocannabinol in rem-sleep-deprived rats.
Carlini EA, Lindsey CJ.
1. delta 9-Tetrahydrocannabinol (THC) induced aggressive behavior in rats previously deprived of REM sleep. This aggressiveness was significantly potentiated by tryptophan and fluoxetine, drugs which increase brain serotonin availability. 2. Conversely, drugs which decrease serotonergic function such as D,L-p-chlorophenylalanine, cinanserin and cyproheptadine strongly blocked the aggressive behavior. 3. On the basis of previous data indicating an involvement of dopaminergic mechanisms in this type of aggressiveness and the present results showing a role for serotonin, it is concluded that REM deprivation-THC aggression is under the control of at least these two neurotransmitters.

In an epidemiological study (Moffitt, et al., 1998), a record of violence was associated with above-average serotonin levels. -Ray Peat, PhD

Biol Psychiatry. 1998 Mar 15;43(6):446-57.
Whole blood serotonin relates to violence in an epidemiological study.
Moffitt TE, Brammer GL, Caspi A, Fawcett JP, Raleigh M, Yuwiler A, Silva P.
BACKGROUND:
Clinical and animal studies suggest that brain serotonergic systems may regulate aggressive behavior; however, the serotonin/violence hypothesis has not been assessed at the epidemiological level. For study of an epidemiological sample we examined blood serotonin, because certain physiological and behavioral findings suggested that it might serve as an analog marker for serotonergic function.
METHODS:
Whole blood serotonin was measured in a representative birth cohort of 781 21-year-old women (47%) and men (53%). Violence was measured using cumulative court conviction records and participants’ self-reports. Potential intervening factors addressed were: gender, age, diurnal variation, diet, psychiatric medications, illicit drug history, season of phlebotomy, plasma tryptophan, platelet count, body mass, suicide attempts, psychiatric diagnoses, alcohol, tobacco, socioeconomic status, IQ, and overall criminal offending.
RESULTS:
Whole blood serotonin related to violence among men but not women. Violent men’s mean blood serotonin level was 0.48 SD above the male population norm and 0.56 SD above the mean of nonviolent men. The finding was specific to violence, as opposed to general crime, and it was robust across two different methods of measuring violence. Together, the intervening variables accounted for 25% of the relation between blood serotonin and violence.
CONCLUSIONS:
To our knowledge, this is the first demonstration that an index of serotonergic function is related to violence in the general population

Article:
LARGE-SCALE STUDY LINKS SEROTONIN LEVELS, AGGRESSION

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By Team FPS – November 5, 2011

Paul Chek – Nutrition: The Dirt Facts

 

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By Team FPS – November 4, 2011

Aspirin and Exercise

Also see:
Benefits of Aspirin
Exercise Induced Stress
Exercise and Effect on Thyroid Hormone
Ray Peat, PhD and Concentric Exercise
Ray Peat, PhD: Quotes Relating to Exercise
Lactate Paradox: High Altitude and Exercise
Carbohydrate Lowers Exercise Induced Stress
Exercise Induced Menstrual Disorders
Synergistic Effect of Creatine and Baking Soda on Performance
Protective Carbon Dioxide, Exercise, and Performance

Eur J Appl Physiol. 2003 Apr;89(2):177-83. Epub 2003 Feb 1.
The influence of aspirin on exercise-induced changes in adrenocorticotrophic hormone (ACTH), cortisol and aldosterone (ALD) concentrations.
Przybyłowski J, Obodyński K, Lewicki C, Kuźniar J, Zaborniak S, Drozd S, Czarny W, Garmulewicz M.
The influence of aspirin (ASA) on the endocrinology system and prostaglandin (PGs) synthesis is not completely clear. The aim of the study was to estimate the influence of ASA on the changes in the concentration of ACTH, cortisol and aldosterone (ALD) induced by physical exercise. This study was conducted on 19 healthy students (age 21-23 years). They were subjected to intensive physical exercise on a cycle ergometer. On the day prior to the experiment, 12 subjects took two 0.5-g doses of ASA in a wafer, and another 0.5 g 3-4 h before the test on the day of the investigation (ASA group). The remaining seven subjects (control group) received placebo. Hematocrit, lactate concentration and concentrations of ACTH, cortisol and ALD were determined before exercise, after exercise, and after 30 min of recovery, in a blood sample taken from a cubital vein. Before exercise, the degree of platelet aggregation in response to arachidonic acid was estimated, in order to confirm the correct allocation to the two groups. Aggregation should only occur in the ASA group. ASA and control groups exercised for 30.3 (3.1) min and 30.2 (1.6) min, respectively. Maximal heart rate and lactate concentration were similar in both groups, as were the basal concentrations of ACTH and cortisol; the ALD concentration seemed lower in the ASA group, but the difference was not significant (p<0.1). In both groups after exercise ACTH, cortisol and ALD concentrations were significantly increased, however when compared to the control group, the increase of ACTH in the ASA group was significantly higher, and ALD increase significantly lower. After recovery there was a significant decrease in ACTH concentration, whereas the concentrations of ALD and cortisol did not change. The concentrations of cortisol in both groups after exercise and recovery were similar. That is most likely because the ACTH concentrations in the ASA and control groups were sufficient for almost maximal cortisol secretion. It is proposed that ASA administration caused prostaglandin synthesis to decrease, and that this led to a lower basal concentration of ALD and a significantly lower level of ALD after exercise.

Int J Sports Med. 2007 Oct;28(10):809-14. Epub 2007 May 11.
Do non-steroidal anti-inflammatory drugs influence the steroid hormone milieu in male athletes?
Di Luigi L, Rossi C, Sgrò P, Fierro V, Romanelli F, Baldari C, Guidetti L.
Prostaglandins modulate the hypothalamus-pituitary-adrenal and -gonadal axis pathways. We explored the effects of a single course of treatment with acetylsalicylic acid (ASA), an inhibitor of prostaglandin synthesis, on the steroid milieu in athletes. Morning plasma cortisol (F), dehydroepiandrosterone sulphate, free-testosterone, testosterone (T) and their ratios were evaluated before and after the administration of either ASA or placebo in twelve male athletes, when affected by minor musculoskeletal trauma and, as control, after a five/six week wash-out in healthy conditions respectively. One tablet of ASA (800 mg), or placebo, was administered two times daily for 10 days during treatment. All the volunteers suspended exercise training during treatment. The results revealed that compared to placebo, plasma F was significantly lower after ASA treatment (p = 0.023). Furthermore, the comparison of hormone’s absolute and percentage of variations (Delta and Delta%) between ASA and placebo treatment showed significant differences respectively for DeltaF (p = 0.045), for DeltaT (p = 0.047), for DeltaT/F (p = 0.042), for DeltaF% (p = 0.04) and for DeltaT% (p = 0.049). Our data suggest that in comparison to placebo, a short-term ASA treatment is able to influence the plasma steroid milieu in athletes. Due to the observed variability of the individual hormonal patterns, further research is required to substantiate these findings.

Med Sci Sports Exerc. 2001 Dec;33(12):2029-35.
Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans.
Di Luigi L, Guidetti L, Romanelli F, Baldari C, Conte D.
Abstract
PURPOSE: Prostaglandins (PGs) modulate the activity of the hypothalamus-pituitary axis, and pituitary hormones are largely involved in the physiological responses to exercise. The purpose of this study was to analyze the effects of acetylsalicylic acid (ASA), an inhibitor of PGs synthesis, in the pituitary responses to physical stress in humans.
METHODS: Adrenocorticotropin (ACTH), beta-endorphin, cortisol, growth hormone (GH), and prolactin (PRL) responses to exercise were evaluated after administration of either placebo or ASA. Blood samples for hormone evaluations before (-30, -15, and 0 pre) and after (0 post, +15, +30, +45, +60, and +90 min) a 30-min treadmill exercise (75% of .VO(2max)) were taken from 12 male athletes during two exercise trials. One tablet of ASA (800 mg), or placebo, was administered two times daily for 3 d before and on the morning of each exercise-test.
RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise. Furthermore, although no differences in the GH response to exercise were shown, a significantly reduced total PRL response to stress condition was observed after ASA.
CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response). Even though it is not possible to exclude direct action for ASA, our data indirectly confirm a role of PGs in these responses. We have to further evaluate the nature of the preexercise endocrine activation and, because of the large use of anti-inflammatory drugs in athletes, whether the interaction between ASA and hormones might positively or negatively influence health status, performance, and/or recovery.

Respir Physiol Neurobiol. 2002 Apr;130(2):189-99.
The post-exercise oxidative stress is depressed by acetylsalicylic acid.
Steinberg J, Gainnier M, Michel F, Faucher M, Arnaud C, Jammes Y.
In order to assess whether oxidative stress occurs after fatiguing dynamic contractions of a small forearm muscle group, we estimated the kinetics of changes in some of its biomarkers (thiobarbituric acid reactive substances or TBARS; plasma reduced ascorbic acid or RAA; erythrocyte reduced glutathione or GSH). We also tested the hypothesis that acetylsalicylic acid (ASA) may compete with endogenous radical targets, attenuating the post-exercise oxidative stress. Seven male subjects successively performed a 3-min dynamic handgrip exercise with the dominant and then the contralateral forearm. Blood samples were taken from an antecubital vein in each exercising forearm. Biochemical analyses, including the concentration measurements of lactic acid, potassium, and oxidative stress markers were performed at rest and then during the 30-min period of recovery following each exercise. The same day, exercises were repeated after ingestion of a single dose (10 mg/kg) of ASA, and the same exercises were performed after a 3-day ASA treatment (30 mg/kg/day). In control condition, the changes in TBARS, RAA and GSH were already significant immediately after the end of the forearm exercise. They culminated after 5 min, and control values were recovered by a 30-min rest period. We verified that repeated bouts failed to alter the post-exercise variations. ASA did not modify the lactic acid production significantly, though the 3-day ASA treatment significantly reduced the efflux of potassium (-74%, P < 0.05), and the post-exercise variations of TBARS (-45%, P < 0.01), RAA (-44%, P < 0.01) and GSH (-48%, P < 0.01). These results suggest that the dynamic handgrip exercise is a good model for studying the post-exercise oxidative stress and also that ASA seems to offer an efficient protection against oxidative stress and the changes in membrane permeability to potassium.

Brazilian Journal of Biomotricity, v. 4, n. 3, p. 206-213, Aug 2010
Aspirin may be an effective  treatment for exercise-induced muscle soreness.
Sahar Riasati, Mehrzad Moghadasi, Ahmad Torkfar, Rahim Shirazinejad ,Hamid Arvin
Delayed onset muscle soreness (DOMS) refers to the skeletal muscle pain that is experienced following eccentric exercise. The aim of the present study was to examine the effect of aspirin supplementation on DOMS after an eccentric exercise. Sixteen healthy female [age, 21.05 ± 3.7 years; body mass index (BMI), 24.03 ± 0.8 kg/m2; (mean ± SD)] participated as subjects in this study. The subjects were assigned to either an experimental (200 mg of aspirin; n=8) or a placebo group (Same dosage of lactose; n=8) using a double-blind research design. Knee range of motion (ROM), perceived pain, thigh circumference and serum activity of the enzyme creatine kinase (CK) were taken before, immediately, 24 and 48 hours after the eccentric exercise. No differences among groups were observed for thigh circumference and ROM before, immediately, 24 and 48 hours after the eccentric exercise. Serum CK levels and pain increased (P<0.05) in the both groups immediately after the eccentric exercise and increased to maximum at 48 hours after the eccentric exercise. The aspirin supplementation decreased (P<0.05) the serum CK levels and pain compare to the placebo group at 24 and 48 hours after the eccentric exercise. In conclusion, aspirin supplementation can be effective to minimize DOMS induced by eccentric exercise.

Eur J Heart Fail (2004) 6 (6)
The effect of aspirin on the ventilatory response to exercise in chronic heart failure
Klaus K.A. Witte and Andrew L. Clark
Introduction: Patients with chronic heart failure (CHF) experience breathlessness and fatigue on exercise. One of the abnormalities seen on maximal exercise testing is an increased ventilatory response to exercise (VE/VCO2 slope). The cause of this is unknown, but is likely to be due to a combination of interacting peripheral and central factors. Recent data have demonstrated a relation between VE/VCO2 slope and prostaglandin levels in contracting muscles. The present study examined the influence of the presence of a potent non-selective prostaglandin inhibitor, aspirin, on the ventilatory response to exercise in a group of patients with CHF.
Methods: We investigated the ventilatory response to exercise of 120 consecutive patients in sinus rhythm attending a specialist heart failure clinic. We excluded those taking clopidogrel (six patients) and those on both warfarin and aspirin or taking other non-steroidal anti-inflammatory agents (five patients). The other 109 patients were grouped according to whether they were taking aspirin (n=52 (48%)) or not (n=57 (52%)). Each patient underwent echocardiography to assess left ventricular function, and exercise testing with metabolic gas exchange to derive peak oxygen consumption (pVO2) and the VE/VCO2 slope.
Results: The groups were similar in terms of age, (67 (13) vs. 66 (12) years; P=0.34) drug use, heart failure aetiology, left ventricular function (ejection fraction; 33.3 (9.4) vs. 31.8 (9.9)%; P=0.05)) and exercise tolerance (pVO2; 20.4 (5.3) vs. 19.9 (6.0); P=0.68, and VE/VCO2 slope; 35.4 (6.2) vs. 35.7 (9.3); P=0.73). There was no difference in the ventilatory response to exercise or the symptoms of breathlessness between the two groups.
Conclusions: Aspirin does not appear to affect exercise performance in CHF.

Circulation 1980, 61:62-65
Production of Circulating Platelet Aggregates by Exercise in Coronary Patients
ANDREW G. KUMPURIS, M.D., ROBERT J. LUCHI, M.D., CAROLINE C. WADDELL, M.D.,
AND RICHARD R. MILLER, M.D.
SUMMARY To determine the effect of exercise on the in vivo formation of circulating platelet aggregates in patients with severe coronary artery disease (CAD), platelet aggregate ratios (PAR) (normal 0.8-1.1) were measured immediately before and after treadmill exercise and 30 minutes after exercise in 17 CAD patients (group 1, mean age 55 years), 12 age-matched normal subjects (group 2), and 13 young normals (mean age 27 years, group 3). Coronary patients had lower resting PAR than group 3 (0.79 ± 0.05 vs 0.98 ± 0.03; p <0.01), while group 2 had an intermediate value 0.86 4- 0.04 (p > 0.05 vs CAD and group 3). Immediately after exercise, group I PAR declined from 0.79 i 0.05 to 0.53 ± 0.04 (p < 0.001), while groups 2 and 3 were unchanged (p > 0.05; both p < 0.001 vs group 1); 30 minutes after exercise, PAR in group 1 rose to 0.66 ± 0.05 (p < 0.05 vs pre- and immediately postexercise); groups 2 and 3 remained unchanged vs pre- and immediately postexercise (p > 0.05; both p < 0.001 vs group 1). Six group 1 patients received 1300 mg aspirin daily for 10 days and repeated the protocol. Resting PARs were unchanged (p > 0.05) from resting values without aspirin. The exercise-induced decline in PAR was attenuated by aspirin: without aspirin, 0.73 ± 0.02 preexercise to 0.54 ± 0.04 postexercise; with aspirin, 0.73 ± 0.03 to 0.82 ± 0.03 (p < 0.05 vs no aspirin). These data indicate that platelet aggregation occurs with exercise in CAD. In addition, these data suggest that as

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By Team FPS – November 3, 2011

Fats and Oils: The significance of temperature

Also see:
Charts: Mean SFA, MUFA, & PUFA Content of Various Dietary Fats
Dietary Fats, Temperature, and Your Body

by Barry Groves

Have you ever wondered why polyunsaturated margarine has to be kept in a fridge, yet coconut oil can be kept out at room temperature for a year or more without any untoward effects? All fats and oils in Nature are a mixture of saturated, monounsaturated and polyunsaturated fatty acids. The only difference between them is the proportions of each. Whether they are in plant or animal tissues, this is governed by the temperature at which the different fats and oils are designed to operate. This point, which is often neglected when discussing the healthiness or otherwise of fats and oils, is actually the most important consideration. The degree of saturation or unsaturation determines not only a fat’s melting point, but also its chemical stability and its likelihood of auto-oxidising and creating harmful free radicals. The higher the proportion of saturated fatty acids a fat is, the less likely it is to go rancid; the more polyunsaturated fatty acids it contains, the more difficult it is to stop it going bad.

In plants, oils are usually found in their seeds. The degree of saturation of plant oils and fats is entirely dependent on the temperature in which they are grown. These oils provide a store of energy for the seeds’ germination, usually in early spring when the weather is cool. For this reason, the energy contained in the oils must be accessible when ambient temperatures are low. Unsaturated oils melt at lower temperatures, and the more unsaturated they are, the lower the temperature at which they are viable. So we find oils that are highly saturated, such as coconut oil, in the tropics; palm oil, which grows slightly further from the equator, is a little less saturated; monounsaturated oils are found in olives grown in Mediterranean regions; and polyunsaturated oils in theseeds of plants grown in cooler climates. It has also been shown that the same plant species grown in a warm climate will be more saturated than if grown in a cooler region.[1]

The same is true of animals. Pigs dressed in sweaters were also found to have more saturated fat than unclothed pigs.[2] Animals must have body fats which are liquid otherwise they would be too stiff to move. So cold blooded animals such as fish, which also live in cold water, contain highly polyunsaturated fatty acids with many double bonds: the EPA and DHA of fish oils have five and six double bonds respectively. But as body or environmental temperatures rise, so we find fats tending to become more saturated. The fats of all warm blooded animals contain mixtures of saturated and unsaturated fatty acids, but the degree of saturation is quite high. Human body fat is naturally about 40% saturated, 57% monounsaturated and only 3% polyunsaturated.

This temperature aspect is highly relevant because any fat or oil must be stable at the temperature at which it is going to be used. If it is attacked by oxygen and goes rancid, as polyunsaturated margarines do if they are not refrigerated, then they become unfit for consumption if they are outside the body, and extremely harmful if they are inside it.

All polyunsaturated fatty acids will auto-oxidise at body temperature unless they are protected in some way. Let’s look at how Nature makes sure it doesn’t happen.

Coconuts are found in equatorial regions where the ambient temperature may be well over 40°C (104°F). Coconut oil contains a small percentage of polyunsaturated fatty acids — but significantly, coconut oil doesn’t go rancid at this temperature as a polyunsaturated margarine very quickly would. This is because the polyunsaturated fatty acids in coconut oil are protected by the very high percentage of saturated fatty acids.

Our body temperature at 37°C (98.6°F) is not really much lower than the coconut’s environment. Our fat must also be both liquid and stable at this temperature. So it, too, contains a high proportion of saturated fat and only a small amount of polyunsaturated fat. Just like the coconut, the saturated fatty acids in our bodies protect the polyunsaturated fatty acids from oxidation. However, if we eat a diet that contains high levels of polyunsaturated fats, as ‘healthy eating’ tells us we should, those fats will be incorporated in our body cells. And that, as we will see later, makes them a recipe for disaster.

Fish, whether in the cold arctic or in warmer waters, contain a higher proportion of polyunsaturated fats than do warm blooded animals. In the tropics, where diets tend to include lots of fish, coconut oil is also eaten in plenty. South Pacific islanders are protected from the harmful effects of the polyunsaturated fats in the fish by the saturated fats in the coconuts. It is also noticeable that human cultures in the tropics eat high levels of saturated coconut oil and they don’t suffer heart disease.

We who live in cooler climates have the same body temperatures as Pacific islanders and we eat animals such as cattle, pigs and sheep. The natural fat of those food animals is very similar to our own fat. If the animals are allowed to feed naturally, the saturated fatty acids in animal fat protect the polyunsaturated element in our diet. This makes the fat of these animals entirely healthy for both them and us. There is one caveat, however: Nowadays, the establishment is trying to make fats ‘healthier’ by feeding animals with commercially produced foodstuffs that contain high levels of polyunsaturated seed oils, notably from soya and maize (corn).

Table I: Fatty Acid Composition of Selected Fats[3] 

Fat or oil Saturated (%) Monounsat (%) Polyunsat (%)
Coconut 91 6 3
Palm kernel 83 16 1
Butter 60 34 6
Human milk 54 39 8
Lamb 53 41 5
Beef 45 51 5
Pork 43 48 8
Human (body fat) 40 57 3
Hen’s Egg 39 47 14
Chicken 35 48 16
Cod 26 16 59
Margarine (polyunsat) 24 21 55
Soya oil 18 24 58
Olive oil 17 74 9
Corn oil 13 24 59
Sunflower oil 10 20 66
Safflower oil 9 12 75
Canola oil 6 67 27

 

In the table above, the figures for food animals are based on animals eating their natural diet as they did when these values were determined. Today, however, many food animals are fed on foods which are more polyunsaturated — and the figures can be very different. For example, pork fat which should be about 8% polyunsaturated, can now be well over 30%.[4] And as many of our intensively farmed food animals are now fed large amounts of grains and soya, it is no longer accurate to speak of their fats as ‘animal fats’; in many cases they are more akin to vegetable oils. In the same way that these are taken up by the animals, when we eat them they are also incorporated in our body cells. That turns what should be a healthy fatty acid profile into a decidedly unhealthy one, with serious implications not only for those animals, but for our health as well.

References

1. Wolf RB. Effect of temperature on soybean seed constituents. J Am Oil Chem Soc 1982; 59: 230-2.
2. Wolfe R. Chemistry of nutrients and world food. Univ of Oregon Chem. October 16, 1986; 121.
3. Paul AA, Southgate DAT. McCance & Widdowson’s The Composition of Foods. Fourth revised extended edition of MRC Special Report, No 297. HMSO, London, 1979.
4. McHenry EW,Cornett ML. The role of vitamins in anabolism of fats. Vit Horm 1944; 2: 1-27.

http://www.second-opinions.co.uk/temperature-of-oils.html

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By Team FPS – November 2, 2011

Dairy, Calcium, and Weight Management in Adults and Children

Also see:
High-fat cheese: the secret to a healthy life?
Cheese: the secret to a longer life and faster metabolism?
The Full-Fat Paradox: Whole Milk May Keep Us Lean
DAIRY – POWERFUL AND UNDERAPPRECIATED FOR FAT LOSS
Calcium Paradox
Source of Dietary Calcium: Chicken Egg Shell Powder
Low CO2 in Hypothyroidism
Blood Pressure Management with Calcium & Dairy
Hypertension and Calcium Deficiency
Excess Dietary Phosphorus Lowers Vitamin D Levels
Fatty Acid Synthase (FAS), Vitamin D, and Cancer
Phosphate, activation, and aging
Parmigiano Reggiano cheese and bone health
Preparing Powdered Eggshells for Calcium
Milk and dairy products: good or bad for human health? An assessment of the totality of scientific evidence.

Quotes by Ray Peat, PhD:
“The ratio of calcium to phosphate is very important; that’s why milk and cheese are so valuable for weight loss, or for preventing weight gain. For people who aren’t very active, low fat milk and cheese are better, because the extra fat calories aren’t needed.”

“Two other ideas that sometimes cause people to avoid drinking milk and eating cheese are that they are “fattening foods,” and that the high calcium content could contribute to hardening of the arteries.

When I traveled around Europe in 1968, I noticed that milk and cheese were hard to find in the Slavic countries, and that many people were fat. When I crossed from Russia into Finland, I noticed there were many stores selling a variety of cheeses, and the people were generally slender. When I lived in Mexico in the 1960s, good milk was hard to find in the cities and towns, and most women had fat hips and short legs. Twenty years later, when good milk was available in all the cites, there were many more slender women, and the young people on average had much longer legs. The changes I noticed there reminded me of the differences I had seen between Moscow and Helsinki, and I suspect that the differences in calcium intake were partly responsible for the changes of physique.

In recent years there have been studies showing that regular milk drinkers are less fat than people who don’t drink it. Although the high quality protein and saturated fat undoubtedly contribute to milk’s anti-obesity effect, the high calcium content is probably the main factor.”

“One of the reasons a lot of people give, if they have overcome the idea that milk forms mucous, or is a risk for diseases and so on; one of their arguments is that it makes them fat. But, all the research on animals, and as far as it goes, human research, shows that milk is probably the best reducing foods there is. The mechanisms for that are now known. Not only the anti-stress effects of casein, and a good balance of saturated fats and so on, but the calcium alone is very important metabolic regulator, that it happens to inhibit the fat-forming enzymes fatty acid synthase, and incidentally that’s a characteristic enzyme that goes wild in cancer. But calcium and milk inhibit that fatty acid synthase, reducing the formation of fats and at the same time it activates the uncoupling proteins in the mitochondria, which are associated with increased longevity. Because they, by increasing the metabolic rate, the uncoupling proteins burn calories faster but they protect against free-radical oxidation. That they pull the fuel through the oxidation process so fast in effect, that none of it goes astray in random oxidation, where if you inhibit your energy producing enzymes you tend to get random, stray oxidation that damage the mitochondria. So the uncoupling proteins burn calories faster, at the same time that your reducing fat synthesis and milk is, as far as I know, they only food does both of those things simultaneously.”

Low dairy intake in early childhood predicts excess body fat gain.
Suboptimal dairy intakes during preschool in this cohort were associated with greater gains in body fat throughout childhood.

Dairy Intake Is Associated with Lower Body Fat and Soda Intake with Greater Weight in Adolescent Girls
Nondairy calcium was not associated with weight or iliac skinfold thickness. Soda intake was significantly positively associated with weight in both models (P = 0.01, both models). Decreasing soda and increasing dairy consumption among Asians may help maintain body fat and weight during adolescence.

Dairy Intake and Anthropometric Measures of Body Fat among Children and Adolescents in NHANES
Among adolescents, suboptimal dairy intake was associated with higher anthropometric measures of body fat.

Dairy food consumption and body weight and fatness studied longitudinally over the adolescent period
Avoidance of dairy foods due to a possible association with relative body weight is not supported by these findings. We find no evidence that dairy food consumption is associated with BMI z-score or %BF during adolescence, but further research specifically designed to address this question is needed.

Dairy calcium intake, serum vitamin D, and successful weight loss
Our study suggests that both higher dairy calcium intake and increased serum vitamin D are related to greater diet-induced weight loss.

Skim milk compared with a fruit drink acutely reduces appetite and energy intake in overweight men and women.
Consumption of skim milk, in comparison with a fruit drink, leads to increased perceptions of satiety and to decreased energy intake at a subsequent meal.

Effect of 1-year dairy product intervention on fat mass in young women: 6-month follow-up.
Dietary calcium intake over 18 months predicted a negative change in body fat mass. Thus, increased dietary calcium intakes through dairy products may prevent fat mass accumulation in young, healthy, normal-weight women.

Fat oxidation and its relation to serum parathyroid hormone in young women enrolled in a 1-y dairy calcium intervention
The results suggest that a chronic diet high in dairy calcium increases whole-body fat oxidation from a meal, and increases in fasting serum PTH relate to decreases in postprandial whole-body fat oxidation.

Increased consumption of dairy foods and protein during diet- and exercise-induced weight loss promotes fat mass loss and lean mass gain in overweight and obese premenopausal women.
The reduction in visceral adipose tissu in all groups was correlated with intakes of calcium (r = 0.40; P < 0.05) and protein (r = 0.32; P < 0.05). Therefore, diet- and exercise-induced weight loss with higher protein and increased dairy product intakes promotes more favorable body composition changes in women characterized by greater total and visceral fat loss and lean mass gain.

The role of dairy foods in weight management.
These data indicate an important role for dairy products in both the ability to maintain a healthy weight and the management of overweight and obesity.

Role of calcium and dairy products in energy partitioning and weight management.
These concepts are confirmed by epidemiologic data and recent clinical trials, which indicate that diets that include > or =3 daily servings of dairy products result in significant reductions in adipose tissue mass in obese humans in the absence of caloric restriction and markedly accelerate weight and body fat loss secondary to caloric restriction compared with diets low in dairy products. These data indicate an important role for dairy products in both the prevention and treatment of obesity.

Role of dietary calcium and dairy products in modulating adiposity.
Further, low-calcium diets impede body fat loss, whereas high-calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. Dairy sources of calcium exert markedly greater effects in attenuating weight and fat gain and accelerating fat loss. This augmented effect of dairy products is likely due to additional bioactive compounds in dairy that act synergistically with calcium to attenuate adiposity. These concepts are confirmed by both epidemiological and clinical data, which demonstrate that increasing dietary calcium results in significant reductions in adipose tissue mass in obese humans in the absence of caloric restriction and markedly accelerates the weight and body fat loss secondary to caloric restriction, whereas dairy products exert significantly greater effects. These data indicate an important role for dairy products in both the prevention and treatment of obesity.

Calcium and dairy products inhibit weight and fat regain during ad libitum consumption following energy restriction in Ap2-agouti transgenic mice.
All 3 high-calcium diets produced significant increases in lipolysis, decreases in fatty acid synthase expression and activity, and reduced fat regain (P < 0.03), but the 2 dairy-containing high-calcium diets exerted significantly greater effects on regain (P < 0.01). Thus, high-Ca diets elicit a shift in energy partitioning and reduction of weight gain during refeeding, with dairy Ca sources exerting markedly greater effects.

Effects of dietary calcium on adipocyte lipid metabolism and body weight regulation in energy-restricted aP2-agouti transgenic mice.
Adipocyte [Ca2+]i was unaffected by Kcal restriction but was reduced markedly by all three high Ca diets (290 vs. 130 nM, p2+]i and thereby reduce energy storage and increase thermogenesis during Kcal restriction.

Normalizing Calcium Intake: Projected Population Effects for Body Weight
Although calcium intake explains only a small fraction of the variability in weight or weight gain, shifting the mean of the distributions downward by increasing calcium intake can be estimated to reduce the prevalence of overweight and obesity by perhaps as much as 60–80%.

Calcium and Weight: Clinical Studies
Analysis reveals a consistent effect of higher calcium intakes, expressed as lower body fat and/or body weight, and reduced weight gain at midlife. Similarly, studies relating nutrient intake to body composition report negative associations between calcium intake and body weight at midlife and between calcium and body fat accumulation during childhood. There is a fairly consistent effect size, with each 300 mg increment in regular calcium intake associated with ∼1 kg less body fat in children and 2.5–3.0 kg lower body weight in adults. Taken together these data suggest that increasing calcium intake by the equivalent of two dairy servings per day could reduce the risk of overweight substantially, perhaps by as much as 70 percent.

Regulation of Adiposity and Obesity Risk By Dietary Calcium: Mechanisms and Implications
Further, low calcium diets impede body fat loss, while high calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. These findings are further supported by clinical and epidemiological data demonstrating a profound reduction in the odds of being obese associated with increasing dietary calcium intake. Notably, dairy sources of calcium exert a significantly greater anti-obesity effect than supplemental sources in each of these studies, possibly due to the effects of other bioactive compounds, such as the angiotensin converting enzyme inhibitor found in milk, on adipocyte metabolism, indicating an important role for dairy products in the control of obesity.

Dairy Product Components and Weight Regulation: Symposium Overview
However, data suggest that both calcium and other dairy product components may contribute to alterations in metabolic partitioning of dietary energy, resulting in modulation of body weight, body fat and the insulin-resistance syndrome.

Human Obesity: Is Insufficient Calcium/Dairy Intake Part of the Problem?
Taken together, these observations suggest that insufficient calcium intake can be part of the obesity problem in some individuals and that an increase in calcium/dairy intake is part of the solution.

Dietary and Total Calcium Intakes Are Associated with Lower Percentage Total Body and Truncal Fat in Young, Healthy Adults
Our findings support a relationship, even after adjusting for physical activity, between higher dietary and total calcium intakes and lower total body and truncal fat in young adults. Results suggest an intake of approximately 1500 mg/d calcium could aid in the management of body and truncal fat. We recommend that young adults be encouraged to increase their total calcium intakes to at least the recommended daily allowance of 1000 mg/d for reasons extending beyond bone health.

Regulation of adiposity by dietary calcium.
Weight gain and fat pad mass were reduced by 26-39% by the three high calcium diets (P<0.001). The high calcium diets exerted a corresponding 51% inhibition of adipocyte fatty acid synthase expression and activity (P<0.002) and stimulation of lipolysis by 3. 4- to 5.2-fold (P<0.015). This concept of calcium modulation of adiposity was further evaluated epidemiologically in the NHANES III data set. After controlling for energy intake, relative risk of being in the highest quartile of body fat was set to 1.00 for the lowest quartile of Ca intake and was reduced to 0.75, 0.40, and 0.16 for the second, third, and fourth quartiles, respectively, of calcium intake for women (n=380;P<0.0009); a similar inverse relationship was also noted in men (n=7114; P<0.0006). Thus, increasing dietary calcium suppresses adipocyte intracellular Ca(2+) and thereby modulates energy metabolism and attenuates obesity risk.

Association between obesity and calcium:phosphorus ratio in the habitual diets of adults in a city of Northeastern Brazil: an epidemiological study
Values above the median for the Ca:P ratio found in the habitual diet were negatively associated with central obesity based on WHtR. In addition, calcium and dairy consumption were negatively associated with central obesity based on WHtR. Therefore, higher Ca:P ratios contributed to a lower prevalence of central obesity.

THE INCREASE OF DAIRY INTAKE IS THE MAIN DIETARY FACTOR ASSOCIATED WITH REDUCTION OF BODY WEIGHT IN OVERWEIGHT ADULTS AFTER LIFESTYLE CHANGE PROGRAM.
de Oliveira EP, Diegoli AC, Corrente JE, McLellan KC, Burini RC
This study evaluated which was the main nutritional change associated with weight reduction of overweight adult participants of a lifestyle change program. It was hypothesized that increases in dairy intake could be an important nutrition intervention in a lifestyle change program. 117 individuals, male (19.5%) and female (80.5%), with a minimum age of 36 years (54.2 ± 10.4). All study participants were enrolled in a lifestyle change program consisting of nutritional counseling and physical activity during 20 weeks. All participants were grouped in three groups according to Body Mass Index (BMI) delta median (-0.87 kg/m2) of individuals that showed weight loss: G1 – lost more than 0.87 kg/m2 of BMI (n = 38); G2 – lost 0 to 0.87 kg/m2 of BMI (n = 36); and G3 – increased BMI (n = 43). G1 increased dairy, fruit and vegetables intake and after forward stepwise multiple regression analysis, it was noted that an increase in dairy product intake of 0.40 servings per day had an impact of 9.6% on the loss of one kg/m2 of BMI. In conclusion, an increase in dairy product intake was the main dietary factor associated with reductions in body weight in overweight adults after 20 weeks of lifestyle change program.

===========================
Calcium and Obesity:
Mol. Nutr. Food Res., 58: 1342–1348. doi: 10.1002/mnfr.201300503
High vitamin D and calcium intakes reduce diet-induced obesity in mice by increasing adipose tissue apoptosis
Igor N. Sergeev and Qingming Song
Scope
Modulation of apoptosis is emerging as a promising antiobesity strategy because removal of adipocytes through this process will result in reducing body fat. Effects of vitamin D on apoptosis are mediated via multiple signaling pathways that involve common regulators and effectors converging on cellular Ca2+. We have previously shown that 1,25-dihydroxyvitamin D3 induces the Ca2+ signal associated with activation of Ca2+-dependent apoptotic proteases in mature adipocytes. In this study, a diet-induced obesity (DIO) mouse model was used to evaluate the role of vitamin D and calcium in adiposity.
Methods and results
DIO mice fed high vitamin D3, high Ca, and high D3 plus high Ca diets demonstrated a decreased body and fat weight gain, improved markers of adiposity and vitamin D status (plasma concentrations of glucose, insulin, adiponectin, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone (PTH)), but an increased plasma Ca2+. High D3 and Ca intakes were associated with induction of apoptosis and activation of Ca2+-dependent apoptotic proteases, calpain and caspase-12, in adipose tissue of DIO mice. The combination of D3 plus Ca was more effective than D3 or Ca alone in decreasing adiposity.
Conclusion
The results imply that high vitamin D and Ca intakes activate the Ca2+-mediated apoptotic pathway in adipose tissue. Targeting this pathway with vitamin D and Ca supplementation could contribute to the prevention and treatment of obesity. However, this potentially effective and affordable approach needs to be evaluated from a safety point of view.

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By Team FPS – November 2, 2011

The Story of Cosmetics

The Story of Cosmetics, released on July 21st, 2010, examines the pervasive use of toxic chemicals in our everyday personal care products, from lipstick to baby shampoo. Produced with Free Range Studios and hosted by Annie Leonard, the seven-minute film by The Story of Stuff Project reveals the implications for consumer and worker health and the environment, and outlines ways we can move the industry away from hazardous chemicals and towards safer alternatives. The film concludes with a call for viewers to support legislation aimed at ensuring the safety of cosmetics and personal care products.

And, for all you fact checkers out there,
http://www.storyofstuff.org/2011/04/14/story-of-cosmetics/

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By Team FPS – October 30, 2011

Big Fat Lies

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By Team FPS – October 29, 2011

GOOD BREATHING, BAD BREATHING

GOOD BREATHING, BAD BREATHING
Breathing is behavior, a unique behavior that regulates body chemistry, pH.
Peter M. Litchfield, Ph.D., May 2006

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By Team FPS – October 28, 2011