Categories:

ATP Regulates Cell Water

Also see:
PUFA Decrease Cellular Energy Production
Gerald Pollack Interviews
Gilbert Ling
Cells, Gels and the Engines of Life
The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor
Protect the Mitochondria
Mitochondrial Medicine

Quotes by Ray Peat, PhD:
“The loss of control over the water in the body is the result of energy failure, and hypertension is one of the adaptations that helps to preserve or restore energy production.”

“As in other cells, ATP maintains the proper water content of cells.”

“…the essential element of stress is the inadequacy of energy to meet a challenge, and when energy is inefficient water is taken up.”

“When a muscle is fatigued, it swells, taking up sodium and water, and it is likely to become sore. Energy depletion causes any cell to take up water and sodium, and to lose potassium. An abnormal excess of potassium in the blood, especially when sodium is low, affects nerve, muscle, and secretory cells; a high level of potassium can stop the heart, for example. Cellular energy can be depleted by a combination of work, insufficient food or oxygen, or a deficiency of the hormones needed for energy production. When the swelling happens suddenly, the movement of water and sodium from the blood plasma into cells decreases the volume of blood, while the quantity of red cells remains the same, making the blood more viscous.”

“When respiration is blocked tissues take up water.”

Science 23 January 1976: Vol. 191 no. 4224 pp. 293-295
What retains water in living cells?
GN Ling, CL Walton
Three types of evidence are presented showing that the retention of cell water does not necessarily depend on the possession of an intact cell membrane. The data agree with the concept that water retention in cells is due to multilayer adsorption on proteins and that the maintenance of the normal state of water relies on the presence of adenosine triphosphate as a cardinal adsorbent, controlling the protein conformations.

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By Team FPS – June 28, 2012

Israeli Paradox: High Omega -6 Diet Promotes Disease

Also see:
Unsaturated Fats, Oxidative Stress, and Atherosclerosis
Unsaturated Fats and Heart Damage
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
PUFA Promote Cancer
Toxicity of Stored PUFA
Dietary PUFA Reflected in Human Subcutaneous Fat Tissue
Arachidonic Acid’s Role in Stress and Shock
Omega 6 Content of Common Foods by Matt Stone

Isr J Med Sci. 1996 Nov;32(11):1134-43.
Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet.
Yam D, Eliraz A, Berry EM.
Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet, a diet that until recently was widely recommended. Despite such national habits, there is paradoxically a high prevalence of cardiovascular diseases, hypertension, non-insulin-dependent diabetes mellitus and obesity-all diseases that are associated with hyperinsulinemia (HI) and insulin resistance (IR), and grouped together as the insulin resistance syndrome or syndrome X. There is also an increased cancer incidence and mortality rate, especially in women, compared with western countries. Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.

Cancer Lett. 1997 Jan 1;111(1-2):179-85.
Subcutaneous, omentum and tumor fatty acid composition, and serum insulin status in patients with benign or cancerous ovarian or endometrial tumors. Do tumors preferentially utilize polyunsaturated fatty acids?
Yam D, Ben-Hur H, Dgani R, Fink A, Shani A, Berry EM.
The relationships between the fatty acid composition of cancerous endometrium and ovary, and peripheral adipose tissues were studied in Israeli Jewish women, and are presented together since no differences were shown between them. The results suggest a mobilization of linoleic acid from subcutaneous and omental depots and its incorporation into tumors accompanied by a high degree of desaturation. High blood insulin concentrations characterized patients with stage I and II disease, and low concentrations characterized patients with advanced degrees of malignancy.

Am J Gastroenterol. 2011 Apr;106(4):563-73. doi: 10.1038/ajg.2011.44.
Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature.
Hou JK, Abraham B, El-Serag H.
OBJECTIVES:
The incidence of inflammatory bowel disease (IBD) is increasing. Dietary factors such as the spread of the “Western” diet, high in fat and protein but low in fruits and vegetables, may be associated with the increase. Although many studies have evaluated the association between diet and IBD risk, there has been no systematic review.
METHODS:
We performed a systematic review using guideline-recommended methodology to evaluate the association between pre-illness intake of nutrients (fats, carbohydrates, protein) and food groups (fruits, vegetables, meats) and the risk of subsequent IBD diagnosis. Eligible studies were identified via structured keyword searches in PubMed and Google Scholar and manual searches.
RESULTS:
Nineteen studies were included, encompassing 2,609 IBD patients (1,269 Crohn’s disease (CD) and 1,340 ulcerative colitis (UC) patients) and over 4,000 controls. Studies reported a positive association between high intake of saturated fats, monounsaturated fatty acids, total polyunsaturated fatty acids (PUFAs), total omega-3 fatty acids, omega-6 fatty acids, mono- and disaccharides, and meat and increased subsequent CD risk. Studies reported a negative association between dietary fiber and fruits and subsequent CD risk. High intakes of total fats, total PUFAs, omega-6 fatty acids, and meat were associated with an increased risk of UC. High vegetable intake was associated with a decreased risk of UC.
CONCLUSIONS:
High dietary intakes of total fats, PUFAs, omega-6 fatty acids, and meat were associated with an increased risk of CD and UC. High fiber and fruit intakes were associated with decreased CD risk, and high vegetable intake was associated with decreased UC risk.

Pharmacology. 2016 Jun 2;98(3-4):134-170. [Epub ahead of print]
Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes.
Okuyama H1, Langsjoen PH, Ohara N, Hashimoto Y, Hamazaki T, Yoshida S, Kobayashi T, Langsjoen AM.
BACKGROUND:
Positive associations have been observed between cardiovascular disease (CVD) and type 2 diabetes mellitus (DM), but their causal relationship has not been clarified. Nevertheless, guidelines from relevant medical societies recommend using cholesterol lowering medication (statin) for both types of patients. Medicines with several different action mechanisms have been developed, and the effectiveness of different lifestyle modifications has been studied extensively for the prevention of DM, which was successful in improving clinical marker status in relatively short-term treatments, but none have been shown to be effective in improving long-term outcomes (mortality from CVD and all causes).
SUMMARY:
Statin-induced suppression of prenyl intermediates in the cholesterol biosynthetic pathway has been linked to stimulated atherosclerosis and heart failure. On the other hand, certain types of vegetable oil and hydrogenated oil shortened the survival of stroke-prone spontaneously hypertensive rats by decreasing platelet number, increasing hemorrhagic tendency and damaging kidney functions, which could not be accounted for by their fatty acid and phytosterol compositions. These vegetable oils and medicines such as statin and warfarin share, in part, a common mechanism to inhibit vitamin K2-dependent processes, which was interpreted to lead to increased onset of CVD, DM, chronic kidney disease, bone fracture and even mental disorder. Impaired vitamin K2-dependent processes by some types of vegetable oils and medicines, but not plasma high low density lipoprotein cholesterol, were proposed as the cause of CVD, DM and other lifestyle-related diseases. High n-6/n-3 fatty acid ratio of ingested foods, but not animal fats, was emphasized to be another risk factor for many of the diseases described above.
KEY MESSAGES:
To date, no randomized controlled trials (RCTs) have been performed to prove the above interpretation. However, the opposite types of RCT trials have been performed by increasing the intake of high-linoleic vegetable oils and reducing that of animal fats, which resulted in increased CVD and all-cause mortality. The amounts of these vegetable oils to exhibit adverse effects in animal studies are not huge (<6 energy %), which should not be overlooked nor disregarded.

J Nutr Biochem. 2016 Nov 4;40:122-131. doi: 10.1016/j.jnutbio.2016.10.016. [Epub ahead of print]
Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse.
Mamounis KJ, Yasrebi A, Roepke TA
A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.

International Science and Investigation journal, [S.l.], v. 5, n. 5, p. 157-168, Nov. 2016
Vegetable Oils Consumption as One of the Leading Cause of Cancer and Heart Disease.
NIKNAMIAN, Soroush; KALAMIAN, Miriam.
This review takes a deep look at increases in the incidence of cancer and heart disease after the introduction of industrial vegetable oils in the world. Most vegetable oils are highly processed and refined products, which completely lack the essential nutrients. Omega-6 Linoleic acid from vegetable oils increases oxidative stress in the body of humans, contributing to endothelial dysfunction and heart disease. The consumption of these harmful oils which are high in mega-6 polyunsaturated fats results in changing the structure of cell membrane which contribute to increasing inflammation and the incidence of cancer.

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By Team FPS – June 28, 2012

Wound Healing: Topical Omega -9 is Superior to the “Essential Fatty Acids”

Also see:
Theurapeutic Honey – Cancer and Wound Healing
Anti-Inflammatory Omega -9 Mead Acid (Eicosatrienoic acid)

Wound Repair Regen. 2004 Mar-Apr;12(2):235-43.
Influence of topical administration of n-3 and n-6 essential and n-9 nonessential fatty acids on the healing of cutaneous wounds.
Cardoso CR, Souza MA, Ferro EA, Favoreto S Jr, Pena JD.
Injury triggers a series of physiological events at the wound site. These include an inflammatory response that is established shortly after the injury, which is then followed by an intense formation of tissue over a period of days. Poly- and monounsaturated fatty acids exert major functions on the inflammatory responses, either in the form of phospholipids anchored in the cell membrane or as soluble lipoic mediators. We present evidence that linolenic (n-3), linoleic (n-6), and oleic (n-9) fatty acids can modulate the closure of surgically induced skin wounds. We found that n-9 fatty acids induced faster wound closure when compared to n-3, n-6, and control. In addition, n-9 fatty acids strongly inhibited the production of nitric oxide at the wound site. A mild improvement on wound closure was observed in the n-6 fatty acid-treated animals concurrent with a peak in nitric oxide production at 48 hours postsurgery. N-3 fatty acid treatment significantly delayed wound closure. Furthermore, we showed that n-3 fatty acid induced a peak in nitric oxide at 3 hours postsurgery and an intense deposition of extracellular matrix after 5 days of treatment. Thus, our results suggest a relevant role and potential therapeutic implication for fatty acids on skin wound healing.

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By Team FPS – June 28, 2012

Coconut Oil and Metabolism in Pigs

Also see:
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase
Metabolism, Brain Size, and Lifespan in Mammals
Unsaturated Fats and Longevity
Ray Peat, PhD Quotes on Coconut Oil
Dietary PUFA Reflected in Human Subcutaneous Fat Tissue
Toxicity of Stored PUFA
Israeli Paradox: High Omega -6 Diet Promotes Disease
PUFA Accumulation and Aging

Arch Tierernahr. 1984 Jan;34(1):19-33.
[Nutritional-physiological effects of dietary fats in rations for growing pigs. 4. Effects of sunflower oil and coconut oil on protein and fat retention, fatty acid pattern of back fat and blood parameters in piglets].
[Article in German]
Berschauer F, Rupp J, Ehrensvärd U.
Rations containing 12% sunflower oil (Ration II) and 12% coconut fat (Ration III) were compared with a control ration (Ration I) in a 34 day experiment with growing boars of the German Landrace breed (12-30 kg body weight). The relationships between DP and ME were held constant for all 3 rations, and because of the higher ME contents of the two fat rations, this was achieved by reducing the feed intake, relative to that of the control ration. Parameters measured were growth, composition at slaughter, the apparent digestibility of the crude nutrients and energy, the N-balance and the concentrations of urea, insulin, glucose, triglyceride and cholesterol in the blood. In comparison to Ration I, the apparent digestibilities of crude protein in Rations II and III were 5 and 4% (p less than 0,05) higher, respectively. There was little difference in the apparent digestibility of crude fat between the Rations II and III. However, large differences in the values were determined depending upon method of extraction. There were little differences in the productive performance of the animals fed the fat diets. The control animals had, however, a 13% lower growth rate (p less than 0,05) when compared at similar ME-intakes. As the energy concentration and the growth rate were higher in groups II and III, the feed conversion efficiency and the ME required per kg growth were approximately 30 and 13% lower than that of the control animals. The efficiency of protein utilization of the animals in group III was 4% higher (p greater than 0.05) and the blood urea concentration 20% lower (p less than 0.05) than that in group II. The values for the control animals were intermediate. A similar result was obtained concerning the fat content of the animals. The fat content of the animals in group III was 15.9% and this was significantly lower (p less than 0.001) than that of 21.1% measured in group II. That of the control animals, 18.6%, was not significantly different from the above values. The differences in feeding over the relatively short period of 34 days lead to marked differences in the fatty acid pattern of the backfat. The contents of myristic acid and linoleic acid were significantly different between group II and III; for the former values of 0.8% and 16.9% were determined, respectively, with corresponding values of 48.7 and 11.3% for the latter.(ABSTRACT TRUNCATED AT 400 WORDS)

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By Team FPS – June 26, 2012

High Fat Diet Lowers Anxiety Response in Rats

Physiol Behav. 1996 Sep;60(3):1039-42.
Short-term consumption of a diet rich in fat decreases anxiety response in adult male rats.
Prasad A, Prasad C.
Short- and long-term changes in the composition of dietary macronutrients [protein (P), carbohydrate (C), and fat (F)] alter neurochemistry and behavior in animals. We examined whether short-term intake of a diet rich in P, C, or F affected their anxiety response (AR). AR of Sprague-Dawley rats was measured in an elevated plus maze. Rats were placed in the black compartment facing the wall opposite the aperture, and the time (max. 360 s) it took to enter the white compartment with all four paws was noted. Rats were fed Purina chow and tap water unless otherwise indicated. On repeated testing (three times on the same day) AR increased and, consequently, most rats spent the entire 360 s in the dark. Whereas most rats exhibited low anxiety response in trial 1, which increased during successive trials (low-high group), some exhibited high initial anxiety that remained unchanged (high-high group). To determine whether macronutrients may alter AR, groups of low-high and high-high rats were tested three times on the same day and then put on a P, C, or F diet for 7 days. On day 8, they were again tested for AR in a single trial and the results compared with those of the third trial of the previous test (preC: 302 +/- 39, post-C: 294 +/- 42, p > 0.05; pre-P: 305 +/- 35, post-P: 297 +/- 43, p > 0.05; pre-F: 321 +/- 17, post-F: 241 +/- 24sec, p = 0.009; n = 30; mean +/- SEM). The results show that a diet rich in F, but not P or C, decreases AR in rats.

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By Team FPS – June 26, 2012

Endotoxin and Behavior

Brain Behav Immun. 2006 Nov;20(6):517-26. Epub 2006 May 2.
Immunity and emotions: lipopolysaccharide increases defensive behaviours and potentiates despair in mice.
Many studies have pointed out the relationships between immunity and depression, supporting a neuroimmune hypothesis of depressive disorders. However, despite the growing interest for such a hypothesis and the amount of clinical and experimental data available, the precise nature of this relationship between immunity and depression remains unclear. The present study aimed to investigate further the link between depression and immunity in mice using the modified version of the forced-swimming test. Based on a two-session test, results from our first experiment showed that endotoxin enhanced active defensive behaviours in mice during the first exposure to water, but was associated with increased immobility (i.e., ‘behavioural despair’) in the subsequent session. In our second experiment, we showed that these effects were blocked by a chronic antidepressant treatment with imipramine. Finally, we suggest a link between immunity and depression, based on the behavioural context in which immune activation takes place. We hypothesize that immune activation, by enhancing reactivity to the negative features of a given situation, increases defensive motivation of subjects, but therefore makes them more vulnerable to the deleterious emotional consequences of failure in defensive strategies.

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By Team FPS – June 26, 2012

Radiation Increases Breast Cancer Incidence

Also see:
Harm of Prenatal Exposure to Radiation
Caffeine and Skin Protection
Topical Vitamin E and ultraviolet radiation on human skin
Preventing Breast Cancer
We Are Giving Ourselves Cancer
Alice Stewart: The woman who knew too much
Breast Cancer
Radiation and Growth – Ray Peat
Bone Density: First Do No Harm
Inflammation from Radiation
Hormonal profiles in women with breast cancer
PUFA Increases Estrogen
PUFA Inhibit Glucuronidation
PUFA Promote Cancer
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
Estrogen and Bowel Transit Time
Progestin and Cancer
Study: Acquired Breast Cancer Risk Spans Multiple Generations
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH

JAMA. 1977 Feb 21;237(8):789-90.
Breast cancer induced by radiation. Relation to mammography and treatment of acne.
Simon N.
This communication reports cases of 16 women in who cancer of the breast developed after radiation therapy for acne or hirsutism, suggesting another group at higher risk than is generally expected for cancer of the breast. It is prudent to regard the carcinogenic effect of radiation on the breast as proportional to dose without a threshold. Mammography in young women should be ordered only selectively, not for screening.

Rev Interam Radiol. 1977 Oct;2(4):199-203.
Cancer of the breast–induction by radiation and role of mammography.
Simon N.
Conflict in the management of cancer of the breast exists. Diagnosis by x-ray mammography provides early effective treatment, but x-ray exposure to the breast is cancerogenic. Prudence requires the use of low dose x-rays in mammography, and limits the use of x-ray mammography in the young. Guide lines for the indications for mammography are changing, and large scale population exposure to radiation should await results of demonstration projects in the United States.

J Am Acad Dermatol. 2006 Dec;55(6):981-9. Epub 2006 Aug 14.
Increased breast cancer risk after radiotherapy for acne among women with skin cancer.
El-Gamal H, Bennett RG.
BACKGROUND:
Radiotherapy was commonly used to treat benign conditions, especially skin diseases, during the first half of the twentieth century. Previous studies have shown that radiotherapy for some of these conditions increases the risk of developing breast cancer. Although breast cancer associated with previous radiotherapy for acne has been reported, no statistically significant correlation has been established.
OBJECTIVE:
The aim of this study was to determine whether radiotherapy for acne is a risk factor for subsequent development of breast cancer.
METHODS:
A retrospective nested case-control study was conducted using the cohort of all patients referred for Mohs micrographic surgery to the senior author (R. G. B.) from 1978 to 2003. The case group consisted of 244 women who were skin cancer patients and who had received radiotherapy for acne. The control group consisted of 244 age-matched women skin cancer patients from the same records randomly selected within the initial Mohs micrographic surgery treatment year. Clinical data from both groups regarding cancer history and radiotherapy were extracted and statistically analyzed.
RESULTS:
Women skin cancer patients who had received radiotherapy for acne have a prevalence of breast cancer of 15% compared with 6.6% in control women skin cancer patients, for an odds ratio (OR) of 2.5 (P = .0033; 95% confidence interval, 1.3-4.6). Increased prevalence is correlated with age at treatment younger than 20 years (age-adjusted OR, 2.9; age-adjusted P = .002), treatment sessions numbering 5 or more (age-adjusted OR, 3.5; age-adjusted P = .005), and treatment year occurring before 1950 (age-adjusted OR, 2.9; age-adjusted P = .00013).
LIMITATIONS:
The data used are based primarily on patient history and physical examinations and are therefore limited by the accuracy of the patient and the caregiver.
CONCLUSION:
Women with skin cancer exposed to previous radiotherapy for acne are significantly more likely to develop breast cancer than their age-matched controls with skin cancer. Therefore all women previously treated for acne with radiotherapy should be identified and closely monitored for subsequent breast cancer development.

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By Team FPS – June 23, 2012

Maternal Ingestion of Tryptophan and Cancer Risk in Female Offspring

Also see:
Nutrition and Brain Growth in Chick Embryos
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
PUFA, Estrogen, Obesity and Early Onset of Puberty
Prenatal Exposure to Radiation Increases Cancer Risk

Hum Reprod. 1999 Aug;14(8):2155-61.
Tryptophan ingestion by pregnant rats induces pituitary and mammary tumours in the adult female offspring.
Santana C, Martin L, Valladares F, Diaz-Flores L, Santana-Herrera C, Milena A, Rodríguez Díaz M.
The present study was designed to evaluate the long-term consequences of tryptophan treatment on the central serotonergic activity in the female offspring of rats, and particularly on serotonin-controlled hormone release. During the second half of gestation, tryptophan (200 mg/kg/day) was given daily by stomach intubation to pregnant rats and the brain concentrations of serotonin and 5-hydroxyindole acetic acid and the plasma concentrations of prolactin, progesterone, oestradiol and luteinizing hormone were quantified in the adult female offspring. The offspring showed an increase in hypothalamic serotonin and serum progesterone and prolactin. In addition, maternal ingestion of tryptophan induced a marked rise in 665-day-old offspring in the incidence of both pituitary prolactinomas (62%) and mammary adenomas (49%). Present data suggest that tryptophan regulates serotonergic differentiation during early development. A transitory modification of the tryptophan concentration in the fetal brain induces a permanent increase in hypothalamic serotonin level and, in addition to modifying the release of prolactin, increases the incidence of tumours in the hypophysis and mammary gland.

In males:
Brain Res. 1997 Nov 7;774(1-2):265-8.
Tryptophan ingestion by gestant mothers alters prolactin and luteinizing hormone release in the adult male offspring.
Martin L, Rodríguez Díaz M, Santana-Herrera C, Milena A, Santana C.
The effect of tryptophan administration to pregnant rats on the development of serotonergic systems and serotonin-related hormones in the offspring was studied. The male offspring of rats treated with tryptophan (200 mg/kg/day) during the second half of gestation showed a 4- to 7-fold increase in serum prolactin 40 and 70 days after birth and a 2-fold increase in serum luteinizing hormone 70 days after birth. The forebrain of adult offspring of tryptophan-treated rats showed an increase in serotonin and 5-hydroxyindoleacetic acid levels. Present data suggest that tryptophan regulates serotonergic differentiation during early development.

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By Team FPS – June 23, 2012

PUFA, Estrogen, Obesity and Early Onset of Puberty

Also see:
Fat Tissue and Aging – Increased Estrogen
Estrogen Related to Loss of Fat Free Mass with Aging
Maternal Ingestion of Tryptophan and Cancer Risk in Female Offspring
Childhood conditions influence adult progesterone levels

Article on subject:
Obesity and Family Stress Blamed As Girls As Young As Five Reaching Puberty

Quotes by Ray Peat, PhD:
“Several of the things which cause early puberty and high estrogen, also tend to work against progesterone synthesis.”

“Low thyroid function, relative over-feeding, and the presence of unsaturated oils in the diet are known to accelerate sexual maturity. Early sexual maturity has been associated with premature aging and early death. Fish, octopuses, mice, humans, and plants offer examples in which reproductive maturity initiates the aging process. Although it used to be said that “hot tropical” people had early puberty, and “cold northern” types had late puberty, the best available data contradict that opinion. The oldest averages for the occurrence of puberty occur in tropical regions. (Figure 3) Mere calorie restriction can delay puberty (and this usually means a low fat diet, for poor people in the developed countries) as can be seen in data from Appalachia; late puberty, accompanied by very low birth weight for babies, is the typical pattern of poverty. Given enough fat (especially vegetable oil, including that in beans and corn), harsh conditions can probably cause earlier puberty. but I don’t know of any clear evidence on this subject.

…

L. C. Strong, who developed strains of mice with high estrogen and a tendency to die of
mammary cancer, found that early sexual maturity was associated with a shorter life-span. Similar observations have been made in humans.”

Mol Cell Biochem. 1998 Nov;188(1-2):5-12.
Timing of dietary fat exposure and mammary tumorigenesis: role of estrogen receptor and protein kinase C activity.
Hilakivi-Clarke L, Clarke R.
The possible association between a high fat diet and increased breast cancer risk has remained controversial. This largely reflects the conflicting data obtained from migrant, case control and animal studies, which generally support this association, and cohort studies which often fail to show a link between fat and breast cancer. The mammary gland is particularly sensitive to estrogens during fetal development, leading us to hypothesize that dietary fat levels during this period may significantly influence breast cancer risk. Using chemically-induced mammary tumors in rats as our experimental model, we have demonstrated the ability of a maternal diet, high in the polyunsaturated fatty acid (PUFA) linoleic acid, to alter mammary gland differentiation, accelerate the onset of sexual maturation, and increase breast cancer risk. The mammary glands of female rats exposed to a high-fat diet in utero have more of the undifferentiated structures (terminal end buds) and fewer of the differentiated structures (alveolar buds) than the glands of rats exposed to a low-fat diet in utero. Furthermore, these mammary glands contain lower levels of total estrogen receptors and have reduced total protein kinase C activity. These effects appear to be mediated by an increase in the serum estradiol levels of pregnancy, which are elevated at least 30% in pregnant dams fed a high-fat diet. Furthermore, the administration of estradiol to pregnant dams produces effects on mammary gland development, onset of puberty and sensitivity to chemical carcinogenesis comparable to those seen in the offspring of rats fed a high fat diet during pregnancy. Our results, thus, support the hypothesis based on epidemiological data that high maternal estrogen levels increase daughters’ breast cancer risk. The results also suggest that a high-fat diet may be an important factor in increasing pregnancy estrogenic activity.

Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9372-7.
A maternal diet high in n – 6 polyunsaturated fats alters mammary gland development, puberty onset, and breast cancer risk among female rat offspring.
Hilakivi-Clarke L, Clarke R, Onojafe I, Raygada M, Cho E, Lippman M.
We hypothesized that feeding pregnant rats with a high-fat diet would increase both circulating 17beta-estradiol (E2) levels in the dams and the risk of developing carcinogen-induced mammary tumors among their female offspring. Pregnant rats were fed isocaloric diets containing 12% or 16% (low fat) or 43% or 46% (high fat) of calories from corn oil, which primarily contains the n – 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The plasma concentrations of E2 were significantly higher in pregnant females fed a high n – 6 PUFA diet. The female offspring of these rats were fed with a laboratory chow from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mammary tumor incidence (60% vs. 30%) and shorter latency for tumor appearance (11.4 +/- 0.5 weeks vs. 14.2 +/- 0.6 weeks) than the offspring of the low-fat mothers. The high-fat offspring also had puberty onset at a younger age, and their mammary glands contained significantly higher numbers of the epithelial structures that are the targets for malignant transformation. Comparable changes in puberty onset, mammary gland morphology, and tumor incidence were observed in the offspring of rats treated daily with 20 ng of E2 during pregnancy. These data, if extrapolated to humans, may explain the link among diet, early puberty onset, mammary parenchymal patterns, and breast cancer risk, and indicate that an in utero exposure to a diet high in n – 6 PUFA and/or estrogenic stimuli may be critical for affecting breast cancer risk.

Oncol Rep. 1998 May-Jun;5(3):609-16.
Maternal genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring.
Hilakivi-Clarke L, Cho E, Clarke R.
Human and animal data indicate that a high maternal estrogen exposure during pregnancy increases breast cancer risk among daughters. This may reflect an increase in the epithelial structures that are the sites for malignant transformation, i.e., terminal end buds (TEBs), and a reduction in epithelial differentiation in the mammary gland. Some phytoestrogens, such as genistein which is a major component in soy-based foods, and zearalenone, a mycotoxin found in agricultural products, have estrogenic effects on the reproductive system, breast and brain. The present study examined whether in utero exposure to genistein or zearalenone influences mammary gland development. Pregnant mice were injected daily with i) 20 ng estradiol (E2); ii) 20 microg genistein; iii) 2 microg zearalenone; iv) 2 microg tamoxifen (TAM), a partial estrogen receptor agonist; or v) oil-vehicle between days 15 and 20 of gestation. E2, genistein, zearalenone, and tamoxifen all increased the density of TEBs in the mammary glands. Genistein reduced, and zearalenone increased, epithelial differentiation. Zearalenone also increased epithelial density, when compared with the vehicle-controls. None of the treatments had permanent effects on circulating E2 levels. Maternal exposure to E2 accelerated body weight gain, physical maturation (eyelid opening), and puberty onset (vaginal opening) in the female offspring. Genistein and tamoxifen had similar effects on puberty onset than E2. Zearalenone caused persistent cornification of the estrus smears. These findings indicate that maternal exposure to physiological doses of genistein mimics the effects of E2 on the mammary gland and reproductive systems in the offspring. Thus, our results suggest that genistein acts as an estrogen in utero, and may increase the incidence of mammary tumors if given through a pregnant mother. The estrogenic effects of zearalenone on the mammary gland, in contrast, are probably counteracted by the permanent changes in estrus cycling.

The population trends toward greater obesity and earlier puberty, both of which are associated with a higher risk of breast cancer, suggest that the war against cancer is far from over. In the 19th century when the incidence of breast cancer was much lower than it is now, puberty usually occurred around the age of 17. In countries with a low incidence of breast cancer, puberty still occurs in the middle to late teens. People who are now 100 generally had puberty years later than girls do now. The biological changes now seen in children in the U.S. suggest that the incidence of degenerative diseases of all sorts is likely to increase as these children grow up. -Ray Peat, PhD

Ethn Dis. 1999 Spring-Summer;9(2):181-9.
Secular trend of earlier onset of menarche with increasing obesity in black and white girls: the Bogalusa Heart Study.
Wattigney WA, Srinivasan SR, Chen W, Greenlund KJ, Berenson GS.
Secular trends in onset of menarche and obesity were examined 14 years apart in two biracial (black-white) cohorts of girls aged 8 to 17 under study for cardiovascular risk. The first cohort (N=1,190, 64% white) was examined in 1978-1979, the second (N=1,164, 57% white) in 1992-1994. The second cohort was heavier in terms of body weight and Rohrer index (weight/height3) than the first (P<0.001), except among black girls aged 12 to 13 years. Subscapular skinfold thickness increased in the second cohort of all ages (P<0.0001), while increases in triceps skinfold were less marked. The onset of menarche occurred at an earlier age in the second cohort compared with the first cohort (P<0.0001), both in black girls (11.4+/-1.3 vs 12.3+/-1.4 years) and white girls (11.5+/-1.3 vs 12.3+/-1.3 years). Furthermore, twice as many girls in the second cohort had reached menarche by ages younger than 12 years (P<0.001). All of these obesity measures were significantly associated with the age of menarche in both cohorts (P<0.001) adjusting for height, race and age at examination. These results suggest that this secular trend toward increasing frequency of early onset of menarche may be the result of increasing obesity noted in girls of both races. Since increases in body fatness and related early onset of menarche are risk factors for disorders in adult life including cardiovascular disease and breast cancer, the secular trend in the increasing incidence of obesity throughout the United States is becoming a major public health problem.

Curr Opin Obstet Gynecol. 2006 Oct;18(5):487-91.
Pubertal development in girls: secular trends.
Kaplowitz P.
PURPOSE OF REVIEW:
To provide an overview of recent studies from the US and other parts of the world that provide conflicting data as to whether there has been a secular trend for earlier onset of puberty and menarche from about 1960 to the present.
RECENT FINDINGS:
Studies from the US suggest a decrease in the age of onset of puberty over the past 40 years of between 0.5 and 1.0 years, with black girls maturing 0.5 to 1 year earlier than white girls. There has been a smaller decrease in the mean age at menarche, on the order of 0.2 years. Northern European countries have not reported such a trend, but several other countries have. The most likely explanation for this trend is an increase in the prevalence of obesity in children.
SUMMARY:
In light of the above trends, the view that onset of any pubertal changes prior to age 8 years requires an extensive evaluation should be reevaluated. The majority of such early-maturing girls are normal girls at the early end of the age distribution for pubertal onset. As much attention should be paid to the rate of progression of pubertal findings as to their age of appearance.

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By Team FPS – June 23, 2012

Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring

Also see:
Hormonal profiles in women with breast cancer
PUFA Promote Cancer
PUFA Inhibit Glucuronidation
PUFA Increases Estrogen
PUFA, Estrogen, Obesity and Early Onset of Puberty
Prenatal Exposure to Radiation Increases Cancer Risk
Maternal Ingestion of Tryptophan and Cancer Risk in Female Offspring
Israeli Paradox: High Omega -6 Diet Promotes Disease

Elevated gestational estrogen and a maternal diet high in polyunsaturates contribute to increased cancer risk in the offspring.

Nutrition. 1999 May;15(5):392-401.
The influence of maternal diet on breast cancer risk among female offspring.
Hilakivi-Clarke L, Clarke R, Lippman M.
The induction of breast cancer is a long process, containing a series of biological events that drive a normal mammary cell towards malignant growth. However, it is not known when the initiation of breast cancer occurs. One hypothesis is that a high estrogenic environment during the perinatal period increases subsequent breast cancer risk. There are many sources of extragonadal estrogens, particularly in the diet. The purpose of this paper is to review the evidence that a high maternal intake of dietary fats increases serum estrogens during pregnancy and increases breast cancer risk in daughters. Our animal studies show that a high maternal consumption of corn oil consisting mainly of linoleic acid (omega-6 polyunsaturated fatty acid, PUFA), increases both circulating estradiol (E2) levels during pregnancy and the risk of developing carcinogen-induced mammary tumors among the female rat offspring. A similar increase in breast cancer risk occurs in female offspring exposed to injections of E2 through their pregnant mother. Our data suggest that the mechanisms by which an early exposure to dietary fat and/or estrogens increases breast cancer risk is related to reduced differentiation of the mammary epithelial tree and increased number of mammary epithelial cell structures that are known to the sites of neoplastic transformation. These findings may reflect our data of the reduced estrogen receptor protein levels and protein kinase C activity in the developing mammary glands of female rats exposed to a high-fat diet in utero. In summary, a high dietary linoleic acid intake can elevate pregnancy estrogen levels and this, possibly by altering mammary gland morphology and expression of fat- and/or estrogen-regulated genes, can increase breast cancer risk in the offspring. If true for women, breast cancer prevention in daughters may include modulating the mother’s pregnancy intake of some dietary fats.

Mol Cell Biochem. 1998 Nov;188(1-2):5-12.
Timing of dietary fat exposure and mammary tumorigenesis: role of estrogen receptor and protein kinase C activity.
Hilakivi-Clarke L, Clarke R.
The possible association between a high fat diet and increased breast cancer risk has remained controversial. This largely reflects the conflicting data obtained from migrant, case control and animal studies, which generally support this association, and cohort studies which often fail to show a link between fat and breast cancer. The mammary gland is particularly sensitive to estrogens during fetal development, leading us to hypothesize that dietary fat levels during this period may significantly influence breast cancer risk. Using chemically-induced mammary tumors in rats as our experimental model, we have demonstrated the ability of a maternal diet, high in the polyunsaturated fatty acid (PUFA) linoleic acid, to alter mammary gland differentiation, accelerate the onset of sexual maturation, and increase breast cancer risk. The mammary glands of female rats exposed to a high-fat diet in utero have more of the undifferentiated structures (terminal end buds) and fewer of the differentiated structures (alveolar buds) than the glands of rats exposed to a low-fat diet in utero. Furthermore, these mammary glands contain lower levels of total estrogen receptors and have reduced total protein kinase C activity. These effects appear to be mediated by an increase in the serum estradiol levels of pregnancy, which are elevated at least 30% in pregnant dams fed a high-fat diet. Furthermore, the administration of estradiol to pregnant dams produces effects on mammary gland development, onset of puberty and sensitivity to chemical carcinogenesis comparable to those seen in the offspring of rats fed a high fat diet during pregnancy. Our results, thus, support the hypothesis based on epidemiological data that high maternal estrogen levels increase daughters’ breast cancer risk. The results also suggest that a high-fat diet may be an important factor in increasing pregnancy estrogenic activity.

[propaganda study: omega -3 compared to omega -6 PUFA. 38% still developed cancer on the omega -3 enriched diet.]
Clin Cancer Res. 2002 Nov;8(11):3601-10.
Dietary modulation of pregnancy estrogen levels and breast cancer risk among female rat offspring.
Hilakivi-Clarke L, Cho E, Cabanes A, DeAssis S, Olivo S, Helferich W, Lippman ME, Clarke R.
PURPOSE:
Against the hypothesis that high estrogen levels in utero increase the risk of developing breast cancer in later life are data showing that pregnancy estrogen levels are significantly higher in Asian women who have low breast cancer risk than in Caucasian women. We investigated whether maternal dietary intake of genistein or n-3 polyunsaturated fatty acids (PUFAs), which are typical to Asian but not Caucasian diet, affect pregnancy estrogen levels and susceptibility to mammary tumorigenesis among offspring.
EXPERIMENTAL DESIGN:
For that purpose, pregnant female Sprague Dawley rats were fed isocaloric AIN-93-based diets containing either at 15 mg (low), 150 mg (medium), or 300 mg (high)/kg genistein/diet or low- or high-fat (16 versus 39% energy from fat) diet composed either of n-3 PUFA menhaden oil or n-6 PUFA corn oil. All diets were switched to regular AIN-93 diet when pups were born.
RESULTS:
Maternal intake of n-3 PUFA diets significantly increased pregnancy 17 beta-estradiol (E2) levels (48% increase when compared with high n-6 PUFA diet; P < 0.0045). High genistein exposure also increased pregnancy estrogen levels, but the increase did not reach statistical significance (P < 0.14). The offspring of high-fat n-3 PUFA-consuming dams were significantly less likely to develop 7,12-dimethylbenz-[a]anthracene-induced mammary tumors (38% of these rats developed tumors during week 17 versus 64% of high n-6 PUFA offspring; P < 0.003). Maternal genistein intake did not affect offspring’s tumor incidence. The mammary glands of high fat n-3 PUFA offspring contained more lobules (P < 0.07) and were thus more differentiated, whereas the glands of high genistein offspring contained more terminal end buds (P < 0.0015), which are the sites of malignant transformation.
CONCLUSIONS:
Our findings indicate that the elevated estrogen levels in the n-3 PUFA mothers were linked to reduced rather than increased breast cancer risk among their offspring, suggesting that other effects of n-3 PUFA may counteract the effects of high fetal estrogenicity on the mammary gland. High maternal genistein intake did not reduce offspring’s breast cancer risk, and therefore high maternal soy intake in Asian women may not be associated with daughters’ low breast cancer risk.

Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9372-7.
A maternal diet high in n – 6 polyunsaturated fats alters mammary gland development, puberty onset, and breast cancer risk among female rat offspring.
Hilakivi-Clarke L, Clarke R, Onojafe I, Raygada M, Cho E, Lippman M.
We hypothesized that feeding pregnant rats with a high-fat diet would increase both circulating 17beta-estradiol (E2) levels in the dams and the risk of developing carcinogen-induced mammary tumors among their female offspring. Pregnant rats were fed isocaloric diets containing 12% or 16% (low fat) or 43% or 46% (high fat) of calories from corn oil, which primarily contains the n – 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The plasma concentrations of E2 were significantly higher in pregnant females fed a high n – 6 PUFA diet. The female offspring of these rats were fed with a laboratory chow from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mammary tumor incidence (60% vs. 30%) and shorter latency for tumor appearance (11.4 +/- 0.5 weeks vs. 14.2 +/- 0.6 weeks) than the offspring of the low-fat mothers. The high-fat offspring also had puberty onset at a younger age, and their mammary glands contained significantly higher numbers of the epithelial structures that are the targets for malignant transformation. Comparable changes in puberty onset, mammary gland morphology, and tumor incidence were observed in the offspring of rats treated daily with 20 ng of E2 during pregnancy. These data, if extrapolated to humans, may explain the link among diet, early puberty onset, mammary parenchymal patterns, and breast cancer risk, and indicate that an in utero exposure to a diet high in n – 6 PUFA and/or estrogenic stimuli may be critical for affecting breast cancer risk.

J Natl Cancer Inst. 1996 Dec 18;88(24):1821-7.
Breast cancer risk in rats fed a diet high in n-6 polyunsaturated fatty acids during pregnancy.
Hilakivi-Clarke L, Onojafe I, Raygada M, Cho E, Clarke R, Lippman ME.
BACKGROUND:
Women who took the synthetic estrogen diethylstilbestrol during pregnancy exhibit an elevated risk of breast cancer, whereas those who suffered from preeclampsia, which is associated with low circulating pregnancy estrogens, exhibit a reduced risk. Since a high-fat diet may increase circulating estrogen levels and possibly breast cancer risk, dietary factors during pregnancy could influence the risk of developing this disease.
PURPOSE:
We tested the hypothesis that consumption of a high-fat diet during pregnancy increases carcinogen-induced mammary tumor incidence in rats.
METHODS:
Pregnant or virgin female Sprague-Dawley rats that had been previously treated with 10 mg 7, 12-dimethylbenz[a]anthracene (DMBA) by oral gavage when 55 days old were assigned to one of two isocaloric diets containing either 16% calories from fat (low-fat) or 43% calories from fat (high-fat) for the length of pregnancy or for the equivalent time of approximately 21 days. There were 20 pregnant and 10 nonpregnant DMBA-treated rats per group. Ten additional pregnant animals (not previously treated with DMBA) per group were used for hormone analysis. The fat source used was corn oil, which is high in n-6 polyunsaturated fatty acids, primarily linoleic acid. The animals were checked for tumors at least once per week by palpation. The tumor size, number, and latency to appearance after carcinogen exposure were recorded. The statistical significance of observed differences was tested by use of appropriate two-sided tests.
RESULTS:
Female rats on different diets had virtually identical food intakes and weight gains during pregnancy. On gestation day 19, serum estradiol levels were approximately twofold higher in rats fed a high-fat diet than in rats fed a low-fat diet (P < .02). The serum insulin levels and insulin/glucose ratios (an index of insulin resistance) in rats fed the high-fat diet were approximately twofold lower than in rats fed the low-fat diet, but the differences did not reach statistical significance (P < .09 and P < .09, respectively). On week 18 following DMBA administration, the number of rats developing mammary tumors was significantly higher in the group exposed to a high-fat diet (40% of animals) than in the group exposed to a low-fat diet (10% of animals) during pregnancy (P < .05). Tumor multiplicity, latency to tumor appearance, and size of tumors upon first detection were similar among the dietary groups. No intergroup differences in the mammary tumor incidence were noted in virgin animals that were exposed to the high- or low-fat diets for an equivalent period of time.
CONCLUSIONS:
Our findings indicate that consumption of a diet high in fat (primarily in the form of n-6 polyunsaturated fatty acids) during pregnancy increases the risk of developing carcinogen-induced mammary tumors, possibly by increasing the pregnancy levels of circulating estrogens.
IMPLICATIONS:
If further studies find that the results from animal model studies are applicable to humans, some human breast cancers may be preventable by dietary manipulations during pregnancy.

Oncol Rep. 1998 May-Jun;5(3):609-16.
Maternal genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring.
Hilakivi-Clarke L, Cho E, Clarke R.
Human and animal data indicate that a high maternal estrogen exposure during pregnancy increases breast cancer risk among daughters. This may reflect an increase in the epithelial structures that are the sites for malignant transformation, i.e., terminal end buds (TEBs), and a reduction in epithelial differentiation in the mammary gland. Some phytoestrogens, such as genistein which is a major component in soy-based foods, and zearalenone, a mycotoxin found in agricultural products, have estrogenic effects on the reproductive system, breast and brain. The present study examined whether in utero exposure to genistein or zearalenone influences mammary gland development. Pregnant mice were injected daily with i) 20 ng estradiol (E2); ii) 20 microg genistein; iii) 2 microg zearalenone; iv) 2 microg tamoxifen (TAM), a partial estrogen receptor agonist; or v) oil-vehicle between days 15 and 20 of gestation. E2, genistein, zearalenone, and tamoxifen all increased the density of TEBs in the mammary glands. Genistein reduced, and zearalenone increased, epithelial differentiation. Zearalenone also increased epithelial density, when compared with the vehicle-controls. None of the treatments had permanent effects on circulating E2 levels. Maternal exposure to E2 accelerated body weight gain, physical maturation (eyelid opening), and puberty onset (vaginal opening) in the female offspring. Genistein and tamoxifen had similar effects on puberty onset than E2. Zearalenone caused persistent cornification of the estrus smears. These findings indicate that maternal exposure to physiological doses of genistein mimics the effects of E2 on the mammary gland and reproductive systems in the offspring. Thus, our results suggest that genistein acts as an estrogen in utero, and may increase the incidence of mammary tumors if given through a pregnant mother. The estrogenic effects of zearalenone on the mammary gland, in contrast, are probably counteracted by the permanent changes in estrus cycling.

Nat Commun. 2012 Sep 11;3:1053.
High-fat or ethinyl-oestradiol intake during pregnancy increases mammary cancer risk in several generations of offspring.
de Assis S, Warri A, Cruz MI, Laja O, Tian Y, Zhang B, Wang Y, Huang TH, Hilakivi-Clarke L.
“To test our hypothesis that maternal exposures during pregnancy to factors such as HF diet or a synthetic E2 lead to breast cancer in several generations, we fed pregnant Sprague–Dawley rats (F0) with either an AIN93G control diet or an isocaloric AIN93G-based high fat diet, containing 43% energy from corn oil, throughout gestation.”
“Maternal exposures to environmental factors during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. Here we investigate whether feeding pregnant rats a high-fat (HF)- or ethinyl-oestradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. We show that mammary tumourigenesis is higher in daughters and granddaughters of HF rat dams and in daughters and great-granddaughters of EE2 rat dams. Outcross experiments suggest that the increase in mammary cancer risk is transmitted to HF granddaughters equally through the female or male germ lines, but it is only transmitted to EE2 granddaughters through the female germ line. The effects of maternal EE2 exposure on offspring’s mammary cancer risk are associated with changes in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and oestrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through epigenetic means.”

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By Team FPS – June 23, 2012