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10 Tips for Better Sleep

Also see:
Better Sleep by Chris Masterjohn, PhD
Sleep and Brain Energy Levels: ATP changes during sleep

Quotes by Ray Peat, PhD:
“Good sleep requires fairly vigorous metabolism and a normal body temperature. In old age, the metabolic rate is decreased, and sleep becomes defective.”

“Since glucose and salt are used to treat shock (intravenous 7.5% salt solutions are effective), it seems appropriate to use carbohydrate (preferably sugar, rather than starch) and salty foods during the night, to minimize the stress reaction. They lower adrenalin and cortisol, and help to maintain the volume and fluidity of blood. Thyroid, to maintain adequate carbon dioxide, is often all it takes to improve the blood levels of salt, glucose, and adrenalin.”

“The metabolic rhythm should correspond to the light-dark rhythm, because darkness is a basic biological stress, and sleep is protective against the stress of darkness. Since TSH has many maladaptive effects, and rises along with prolactin and cortisol during the night, some thyroid taken at bedtime helps to reduce the stress, moderating the TSH rise while keeping the blood sugar from falling too fast. Ice cream (i.e., sugar and fat with a little protein) at bedtime has a similar effect, reducing the rise of adrenaline, cortisol, etc., with the result that the morning cortisol peak will be lower, preferably below the middle of the common range, and then it should decline in the afternoon.”

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Energy production and resting body temperature regulate many functions. Ample energy is required to relax fully and sleep deeply. The key to quality sleep is high energy metabolism and maintaining optimal body temperature (98-98.6F). Children sleep well because of their ability to maintain a high body temperature and produce energy and carbon dioxide. The combination of these factors lead to restful sleep rather than inflammatory or stressful sleep.

Disturbed rest is associated with aging, obesity, menopause, depression, and other health problems. If sleep quality is poor, the basis for the issue is an energy problem. As efficient energy production fails (as in hypothyroidism), compensatory mechanisms kick in to prop up the metabolism and the falling body temperature. This compensation involves stress substances that provoke a wide variety of symptoms, among them insomnia or other sleep issues. Here is a brief list of some signs or symptoms of poor sleep quality:

  • Waking unrested or groggy
  • Nocturnal urination
  • Night sweats
  • Difficulty going to sleep
  • Difficulty getting back to sleep if awoken
  • Low waking temperature and pulse
  • Resting temperature or pulse falls after eating breakfast
  • Waking once or more during the night
  • Waking with a rapid heart beat
  • Waking with inflammation, swelling, or coldness especially in hands or feet
  • Snoring
  • Sleep apnea
  • Mouth breathing or waking with dry mouth
  • Nightmares
  • Waking with no appetite

All of the following sleep-enhancing tips promote the production of energy and a reduction in substances that increase stress and inefficient energy production.

1. Eat something salty before bed.
Sodium lowers several stress mediators that can rise during sleep including serotonin, adrenaline, cortisol, and aldosterone. Salt optimizes the blood volume and circulation essential for the delivery of oxygen and nutrients, helps stabilize blood sugar, increases or maintains the body temperature, and raises the production of carbon dioxide (see #8 in this list). A canning and pickling salt added to food, a sugary beverage, or in bone broth eaten before bed is a good way lower inflammatory nocturnal substances.

2. Eat something sugary before bed.
Like sodium, sugar is anti-stress and raises the body temperature. Ripe fruits, fresh orange juice, or milk are good sources of sugar before bed. These carbohydrate choices also contain anti-stress minerals (magnesium, potassium, and calcium) that benefit energy production and sleep quality. Fresh juice with some salt and gelatin added is a good combo, and to make it more potent coconut oil eaten off a spoon can help produce energy efficiently and balance the bloods sugar. Starchy carbohydrates should be avoided because they make blood sugar balance difficult.

Milk with a little sugar and a pinch or more of pickling salt added is a pre-sleep cocktail that has proven successful with my clients and myself. The casein in milk is anti-stress, and the calcium in milk is pro-metabolism and can regulate blood pressure while lowering parathyroid hormone (PTH), which plays a role in some cases of insomnia when elevated. Tips #1 and #2 can assist you with going back to sleep if you happen to awaken one or more times during the night.

3. Eat less meat later in the day.
Meats are rich in tryptophan, which is the precursor to the stress substances serotonin and melatonin. Although generally seen as substances to increase to improve sleep by mainstream standards, these stress substances lower metabolism and disrupt restful, regenerative sleep. This means do not supplement with melatonin or 5-HTP supplements.

By consuming foods deficient in tryptophan later in the day, you can minimize the the nocturnal production of serotonin and melatonin. Foods high in tryptophan are meats, whey protein, and egg whites. Cheese lacks tryptophan because the whey has been removed. Milk does contain tryptophan, but its other nutritional properties seems to offset its tryptophan content. Food, supplement, or food additives (carrageenan for instance) that inflame the intestines increase serotonin. High cortisol from stress, exercise, or blood sugar imbalances can increases serotonin as well.

High meat consumption relative to calcium intake from dairy or eggshell powder can disrupt calcium metabolism and cause a rise in parathyroid hormone, which is associated with sleep problems. This is another reason to be careful with over consumption of meat if you’re having sleep difficulties.

A gelatin supplement and broth contain no tryptophan and are high in glycine making them an is an excellent choice. Add a little butter and salt to broth for a sleep-inducing combo. Having broth or gelatin at meals containing meat during the day and night can help safeguard against poor sleep by providing a more balanced, anti-stress amino acid profile.

4. Use light therapy right up until bed time.
Light is essential for a high rate of metabolism. Our best defense against the stress from the onset of darkness is youthful, restorative sleep. As soon as the sun goes down, metabolism falls and stress substances that harm can sleep quality begin to rise. Darkness damages the energy producing structures (mitochondria) of the cell and (red) light from the sun or bright light supplementation restores them. Red light also activates a key enzyme, cytochrome oxidase, needed for energy production. Shine one to three bright incandescent lights (250 watt BR40 bulb with 10” metal surround) on your skin continuously or intermittently from sunset until bed time to keep the metabolism revved up and stress hormones at bay. Light therapy can also be used during the day if you unable to get outside or if daylight hours are short like during the fall and winter.

5. Balance your blood sugar from the first to your last meal.
Eating imbalanced meals or eating too infrequently degrades sleep quality because of the stress response that results and if chronic enough, the metabolic suppression that occurs. Eating frequently and consuming digestible meals that contain both a protein source (something from an animal) and something from a plant (a carbohydrate) promote balanced blood sugar.

A balanced meal will generally allow you go 3 to 5 hours comfortably without feeling hungry. Anything shorter than that may be a sign that your meal balance or food choices need adjustment. Sipping fresh orange juice, milk, or a homemade shake during the day is a simple way to balance the blood sugar and keep stress substances from interfering with energy production.

6. Use raw carrot (salad) or bamboo shoots daily to reduce endotoxin.
Endotoxin made by bacteria in the intestines are responsible for systemic inflammatory responses in the body. During any type of stress, like darkness or low blood sugar for instance, endotoxin enter the blood stream and promote the stress reaction (rises in histamine, estrogen, tumor necrosis factor, serotonin, and cortisol). Bamboo shoots, raw carrot (salad), aged cascara sagrada, a digestible diet, cholesterol, at least one daily bowel movement, fructose, aspirin, and saturated fats are protective against endotoxin. The raw carrot and bamboo shoot therapies also help support the removal of estrogen, a stress hormone that decreases efficient energy production. Estrogen is in birth control and hormone replacement therapy (HRT). Using these classes of drugs can distort sleep quality, energy production, and hormone balance.

Raw Carrot Salad
C = 8g P = 1g F = 9g
117 calories per serving
Serves 1

Ingredients:
½ to 1 medium carrot
1 t olive oil
1 t refined coconut oil (or additional 1 t olive oil)
½ t favorite vinegar
Pinch of canning and pickling salt

Instructions:
1. Wash carrot thoroughly.
2. Shred carrot vertically and put in bowl.
3. Mix in remaining ingredients. If coconut oil is hard, melt slightly.
4. Pour dressing on carrot salad.

7. Avoid exercise later in the day.
Workouts raise a multitude of stress substances. Exercise depletes glycogen used to balance blood sugar while sleeping and promotes hyperventilation (excess loss of carbon dioxide). If exercise is chronically excessive, it can decrease reproductive hormones that promote sleep quality and suppress thyroid hormone synthesis.

Exercise is least stressful when the body is most resilient and resting temperature and pulse is at its highest (during the afternoon from 11 to 3 pm usually). Regardless of the time of your session, having baking soda and aspirin with vitamin k prior to a session and sugar before, during, and after can reduce the stress from exercise.

8. Use carbon dioxide therapies.
Carbon dioxide is an often forgotten anti-stress substance. Many poor sleepers lack carbon dioxide, which is essential to energy metabolism and oxygenating the cells of the body (Bohr Effect). Carbon dioxide inhibits the release of serotonin (see #3) and directly opposes stress-promoting lactic acid.

The hypothyroid tend to be deficient in CO2. Using carbon dioxide therapies during the day and at night such as bag breathing, drinking carbonated water, a baking soda bath, or consuming baking soda off the spoon on in a beverage can be useful. Buteyko breathing techniques like mouth taping or improving the control pause are other therapies to research.

9. Limit PUFA.
Polyunsaturated fats (PUFA) are promoted as the “healthy fats” and “essential fats” yet they are universally toxic to human physiology and poison our energy production at multiple points, suppress immune function, lower the body temperature, harm the brain and heart, inhibit protein digestion, promote estrogen and cancer, shorten lifespan, and negatively affect our detoxification systems. PUFA also serve as the basis by which toxic and inflammatory breakdown products are made such as prostaglandins, isoprostanes, and lipid peroxides. Excess consumption of PUFA will not only degrade sleep quality, but they are silently a figure head in the rise in obesity and chronic disease in the western world.

Examples of PUFA:

  • Soy oil
  • Corn oil
  • Safflower oil
  • Canola Oil (used in cooking at Whole Foods Market)
  • Fish oil (DHA/EPA) supplements
  • Fatty fish
  • Flax Oil/Linseed Oil
  • Walnut Oil
  • Almond Oil
  • Grains
  • Above ground vegetables
  • Beans
  • Nuts
  • Any nut, seed, bean, or vegetable oil
  • Industrially fed chickens and pigs

PUFA are found in all natural foods so avoiding them completely is impossible. However, consuming foods rich in saturated fats offer protection against the toxicity of the PUFA you eat and the PUFA stored in your tissues. Saturated fats are best for humans since these fats are stable at temperature and when exposed to oxygen.

Examples of saturated fats:

  • Chocolate fats
  • Refined coconut oil
  • Butter
  • Ghee
  • Dairy
  • Ruminant fat (buffalo, cow, goat, lamb, deer)
  • Grass fed eggs
  • Pastured or wild animal fats

10. Be careful with fermented foods.
Lactic acid is produced by cells during stress and also by bacteria in fermented foods. In either case, the liver is responsible for converting lactic acid into glucose. This process requires the use of fuel stored in the liver (glycogen). When available, glycogen is used during sleep to maintain the blood sugar so depleting it with fermented foods affects sleep quality and duration. To avoid this energy burden on the liver, reduction or elimination of fermented foods like kombucha, alcohol, yogurt, sauerkraut, and homemade fermented anything is a good idea. If you find yourself waking during the night, kick some of the fermented foods in your diet to curb for a while to see if your sleep improves.

Summary
This list is not meant to be exhaustive. When health issues are considered a deficiency of energy, many useful and simple therapies are available. The tips listed here extend to correction of more health problems than just sleep issues.

Charting your resting temperature and 60s pulse upon waking while lying in bed, 30-40 minutes after breakfast, and in the afternoon between 12 and 2 pm can give you feedback about whether your dietary and lifestyle strategies are positively or negatively affecting your energy production. The body is capable of overcoming any health issue if given enough energy & supporting nutrients. Many thanks to Ray Peat, PhD for opening my eyes and others to a new, optimistic perspective on health.

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By Team FPS – June 12, 2012

Altitude Improves T3 Levels

Also see:
Protective Altitude
Lactate Paradox: High Altitude and Exercise
Altitude Sickness: Therapeutic Effects of Acetazolamide and Carbon Dioxide
Protective Carbon Dioxide, Exercise, and Performance
Synergistic Effect of Creatine and Baking Soda on Performance
Ray Peat, PhD on Carbon Dioxide, Longevity, and Regeneration

The altitude itself helps the thyroid to function normally. For example, one study (Savourey, et al., 1998) showed an 18% increase in T3 at a high altitude, and mitochondria become more numerous and are more efficient at preventing lactic acid production, capillary leakiness, etc. -Ray Peat, PhD

Eur J Appl Physiol Occup Physiol. 1998;77(1-2):37-43.
Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level.
Savourey G, Garcia N, Caravel JP, Gharib C, Pouzeratte N, Martin S, Bittel J.
High altitude residence is known to modify body biochemistry and hormone status. However, the effects of such a sojourn on these status observed at sea level both immediately and later after return are not as well established as are the effects of an intermittent acclimation. The aim of this study was therefore to investigate these changes. To achieve our objectives, nine subjects received intermittent acclimation at low pressure in a barometric chamber (8 h daily for 5 days, day 1 at 4500 m, day 5 at 8500 m) before an expedition to the Himalayas. Hormonal and biochemical changes were studied using samples of venous blood taken at sea level before and after acclimation, after return from the expedition and 1 and 2 months after descent. Concentrations of thyroid hormones, adrenaline, noradrenaline (NA), hormones of hydromineral metabolism (aldosterone, renin, arginine vasopressin, atrial natriuretic peptide) as well as prolactin, cortisol, insulin and endothelin 1 were measured. Biochemical measurements made were plasma osmolality, and concentrations of glucose, total cholesterol, total proteins, pre-albumin, transferrin, complement 3C, apolipoproteins A1 and B and serum iron. Acclimation induced no alteration in hormone (except for NA with increases of about 1.5, fold P < 0.05) and biochemistry data. After the expedition, hormone responses were characterized by a higher total triidothyronine concentration (+18%, P < 0.05) while other hormones did not vary. A linear relationship was found between thyroid-stimulating-hormone and body mass changes after the expedition (r = 0.67, P < 0.05). The observed increased concentrations of plasma proteins and total cholesterol (P < 0.05) could be related to the restoration of lean body mass. At 1 and 2 months after return, no changes in hormones were observed but a significant decrease in transferrin concentration was noticed. The higher serum iron concentration reported after 1 month (P < 0.05) could have been the result of a physiological haemolysis. It was concluded that both acclimation and the expedition in the Himalayas affected hormone status and body biochemistry status even though the observed changes were slight and rapidly reversed.

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By Team FPS – June 7, 2012

Adrenaline: Decreases T3, Increases Reverse T3

Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3 (Nauman, et al., 1980, 1984). -Ray Peat, PhD

Eur J Clin Invest. 1980 Jun;10(3):189-92.
In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart.
Nauman A, Kamiński T, Herbaczyńska-Cedro K.
Infusion of adrenaline in healthy dogs in a dose simulating spontaneous release of the catecholamine during experimental myocardial infarction produced a significant decrease in the conversion of thyroxine (T4) to triiodothyronine (T3) and a moderate increase in the conversion of T4 to reverse-triiodothyronine (rT3). Similar changes in deiodination of T4 to T3 and to rT3 were also observed when adrenaline was added in vitro to liver and heart homogenates. These results are consistent with a direct effect of adrenaline on T4 deiodination as degradation of exogenous T4, T3 and rT3 was only slightly increased under the experimental condition employed. The present study suggests that increased tissue exposure to adrenaline might contribute to the hormonal changes seen in at least some case of the ‘low T3 syndrome’.

Horm Metab Res. 1984 Sep;16(9):471-4.
The effect of adrenaline pretreatment on the in vitro generation of 3,5,3′-triiodothyronine and 3,3′,5′-triiodothyronine (reverse T3) in rat liver preparation.
Nauman A, Porta S, Bardowska U, Fiedorowicz K, Sadjak A, Korsatko W, Nauman J.
The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the “low T3 syndrome”. Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5′-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.

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By Team FPS – June 7, 2012

Inflammatory TSH

Also see:
W.D. Denckla, A.V. Everitt, Hypophysectomy, & Aging
Removal of the Pituitary: Slows Aging and Hardening of Collagen
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
Thyroid Insufficiency. Is Thyroxine the Only Valuable Drug?
High T4 Concentrations in the Brain – Suppression of Brain Metabolism
Assessment of the Thyroid: Achilles Tendon Reflex
Thyroid Status and Cardiovascular Disease
The Cholesterol and Thyroid Connection
High Blood Pressure and Hypothyroidism
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns
High Cholesterol and Metabolism
Growth Hormone and Edema

Quotes by Ray Peat, PhD
“TSH has direct actions on many cell types other than the thyroid, and probably contributes directly to edema (Wheatley and Edwards, 1983), fibrosis, and mastocytosis. If people are concerned about the effects of a TSH “deficiency,” then I think they have to explain the remarkable longevity of the animals lacking pituitaries in W.D. Denckla’s experiments, or of the naturally pituitary deficient dwarf mice that lack TSH, prolactin, and growth hormone, but live about a year longer than normal mice (Heiman, et al., 2003). Until there is evidence that very low TSH is somehow harmful, there is no basis for setting a lower limit to the normal range.”

“W.D. Denckla discovered that the pituitary hormones are in some way able to accelerate the process of aging…Removing animals’ pituitaries, Denckla found that their aging was drastically slowed.”

“Denckla’s experiments are reminiscent of many others that have identified changes in pituitary function as driving forces in aging and degenerative diseases.”

“When W. Donner Denckla demonstrated that the removal of an animal’s pituitary (or, in the case of an octopus, its equivalent optic gland) radically extended the animal’s life span, he proposed the existence of a death hormone in the pituitary gland.”

“While Arthur Everitt, Verzar, and others were studying the effects of the rat’s pituitary (and other glands) on collagen, W. D. Denckla investigated the effects of reproductive hormones and pituitary removal in a wide variety of animals, including fish and mollusks. He had noticed that reproduction in various species (e.g., salmon) was quickly followed by rapid aging and death. Removing the pituitary gland (or its equivalent) and providing thyroid hormone, he found that animals lacking the pituitary lived much longer than intact animals, and maintained a high metabolic rate. Making extracts of pituitary glands, he found a fraction (closely related to prolactin and growth hormone) that suppressed tissue oxygen consumption, and accelerated the degenerative changes of aging…A high level of respiratory energy production that characterizes young life is needed for tissue renewal. The accumulation of factors that impair mitochondrial respiration leads to increasing production of stress factors, that are needed for survival when the organism isn’t able to simply produce energetic new tissue as needed. Continually resorting to these substances progressively reshapes the organism, but the investment in short-term survival, without eliminating the problematic factors, tends to exacerbate the basic energy problem. This seems to be the reason that Denckla’s animals, deprived of their pituitary glands, but provided with thyroid hormone, lived so long: they weren’t able to mobilize the multiple defenses that reduce the mitochondria’s respiratory energy production.”

“The “little mouse,” and the experiments of Denckla and Everitt, show that a simple growth hormone deficiency or lack of pituitary function can double the life span: Intervention in the many other self-stimulating excitatory pathways can produce additional retardation of the aging process, acting at many levels, from from the extracellular matrix to the brain.”

“A mutant dwarf mouse, called “little”, has only 5% to 10% as much growth hormone as normal mice, and it has an abnormally long lifespan.”

“The metabolic rhythm should correspond to the light-dark rhythm, because darkness is a basic biological stress, and sleep is protective against the stress of darkness. Since TSH has many maladaptive effects, and rises along with prolactin and cortisol during the night, some thyroid taken at bedtime helps to reduce the stress, moderating the TSH rise while keeping the blood sugar from falling too fast. Ice cream (i.e., sugar and fat with a little protein) at bedtime has a similar effect, reducing the rise of adrenaline, cortisol, etc., with the result that the morning cortisol peak will be lower, preferably below the middle of the common range, and then it should decline in the afternoon.”

Endocrine. 2003 Feb-Mar;20(1-2):149-54.
Body composition of prolactin-, growth hormone, and thyrotropin-deficient Ames dwarf mice.
Heiman ML, Tinsley FC, Mattison JA, Hauck S, Bartke A.
Ames dwarf mice have primary deficiency of prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH), and live considerably longer than normal animals from the same line. In view of the documented effects of GH, PRL, and thyroid hormones on lean and fat body mass and skeletal growth, and the suspected relationship of body size and composition to life expectancy, it was of interest to examine age-related changes in body composition of Ames dwarf mice. Lean mass, fat mass, bone area, and bone mineral content (BMC) were determined in dwarf and normal mice at the ages of 2, 4.5 6, and 18 mo using dual X-ray absorptiometry. In addition to the expected significant declines in lean mass, bone area, and BMC, dwarf mice exhibited attenuation of the age-related increase in bone mineral density and delayed or attenuated increase in percentage of body fat. Percentage of body fat was lower in adult dwarfs than in the corresponding normal controls. Patterns of age-related changes in body composition in Ames dwarf mice are consistent with the recent report of age-related changes in body composition in PRL receptor knockout mice. We suspect that reduction in relative adiposity may contribute to the previously reported increase in insulin sensitivity of Ames dwarf mice and thus may be a factor in delayed aging and increased longevity of these animals.

“W.D. Denckla’s version of programmed aging proposed that the pituitary gland was the agent of this programmed aging. He based his idea on the observation that when animals were kept on a semi-starvation diet, starting before puberty, their puberty was delayed and they lived longer than normal, and on later studies showed that when animals’ pituitary glands were removed before puberty, they lived much longer than normal, and all of their tissues and systems aged at a much slower rate. The implication was that if the gland is present and causes aging, its evolutionary purpose is to cause aging, as well as the other process such a reproduction.

The particular function that Denckla focused on as an index of aging was oxygen consumption, which decreases by more than 70% between puberty and old age. He showed that the decrease of oxygen consumption was much less when the pituitary gland was removed, if the animal was given the amount of thyroid hormone that it would normally produce. He found fairly specific pituitary extracts that decreased oxygen consumption, inhibiting the effects of the thyroid hormone, but he never identified a particular pituitary hormone as the antirespiratory aging hormone, or the mechanism responsible for the extract’s effects.” -Ray Peat, PhD

J Clin Invest. 1974 February; 53(2): 572–581.
Role of the pituitary and thyroid glands in the decline of minimal O2 consumption with age.
W D Denckla
Resting O2 consumption rate (BMR) or minimal O2 consumption rate (MOC) declines with age. Data are presented that suggest that a newly described function of the pituitary may be responsible for a considerable part of the total 75% decline in the MOC with age. The new function appears to decrease the responsiveness of peripheral tissues to thyroid hormones. Response curves to injected thyroxine indicated that immature rats were three times more responsive to thyroxine than adult rats. All the major endocrine ablations were performed in this and earlier work, and only pituitary ablation (a) restored in adults part of the responsiveness to thyroxine found in immature rats and (b) arrested the normal age-associated decrease in responsiveness to thyroxine in immature rats. Bovine pituitary extracts were found that decreased the responsiveness of immature rats to thyroxine. Experiments with the new pituitary function suggested a possible endocrine mechanism to explain why partial starvation doubled the lifespan for rats only when started before puberty.

Fed Proc. 1975 Jan;34(1):96.
Pituitary inhibitor of thyroxine.
Denckla WD.
A description is given of a new pituitary function. It is suggested that the new function acts to decrease gradually the responsiveness of the peripheral tissues to thyroid hormones throughout life. It is suggested that the postulated relative hypothyroidism of older animals might contribute to their loss of viability.

Clin Endocrinol (Oxf). 1983 Jun;18(6):627-35.
Mild hypothyroidism and oedema: evidence for increased capillary permeability to protein.
Wheatley T, Edwards OM.
Nine female patients with normal serum total thyroxine (T4) and triiodothyronine (T3) but elevated thyroid stimulating hormone (TSH) levels were studied. Six patients had generalised oedema associated with maximal diurnal weight gains in excess of 1.4 kg. Under conditions of forced water diuresis, before and during physiological replacement of 1-thyroxine, the supine transcapillary escape rate of albumin (TERA) was measured, while the venous colloid osmotic pressure (COP), packed cell volume (PCV) and urinary excretion of water and electrolytes were studied in both the supine and upright positions. The TERA, diurnal weight gain and orthostatic increase in COP fell significantly with treatment. In the six patients with oedema and excessive diurnal weight gains, the retention of salt and water on tilting was reduced with thyroxine treatment. In female patients we consider generalised oedema associated with excessive diurnal weight gain, to be a common and early symptom of hypothyroidism, meriting thyroxine replacement therapy.

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By Team FPS – June 7, 2012

Nutrient Content of Milk Varieties

Nutrient Content of Milk Varieties

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By Team FPS – June 7, 2012

Minimum amount of physical activity for reduced mortality and extended life expectancy

Also see:
Potential Adverse Cardiovascular Effects from Excessive Endurance Exercise

Lancet. 2011 Oct 1;378(9798):1244-53. Epub 2011 Aug 16.
Minimum amount of physical activity for reduced mortality and extended life expectancy: a prospective cohort study.
Wen CP, Wai JP, Tsai MK, Yang YC, Cheng TY, Lee MC, Chan HT, Tsao CK, Tsai SP, Wu X.
BACKGROUND:
The health benefits of leisure-time physical activity are well known, but whether less exercise than the recommended 150 min a week can have life expectancy benefits is unclear. We assessed the health benefits of a range of volumes of physical activity in a Taiwanese population.
METHODS:
In this prospective cohort study, 416,175 individuals (199,265 men and 216,910 women) participated in a standard medical screening programme in Taiwan between 1996 and 2008, with an average follow-up of 8·05 years (SD 4·21). On the basis of the amount of weekly exercise indicated in a self-administered questionnaire, participants were placed into one of five categories of exercise volumes: inactive, or low, medium, high, or very high activity. We calculated hazard ratios (HR) for mortality risks for every group compared with the inactive group, and calculated life expectancy for every group.
FINDINGS:
Compared with individuals in the inactive group, those in the low-volume activity group, who exercised for an average of 92 min per week (95% CI 71-112) or 15 min a day (SD 1·8), had a 14% reduced risk of all-cause mortality (0·86, 0·81-0·91), and had a 3 year longer life expectancy. Every additional 15 min of daily exercise beyond the minimum amount of 15 min a day further reduced all-cause mortality by 4% (95% CI 2·5-7·0) and all-cancer mortality by 1% (0·3-4·5). These benefits were applicable to all age groups and both sexes, and to those with cardiovascular disease risks. Individuals who were inactive had a 17% (HR 1·17, 95% CI 1·10-1·24) increased risk of mortality compared with individuals in the low-volume group.
INTERPRETATION:
15 min a day or 90 min a week of moderate-intensity exercise might be of benefit, even for individuals at risk of cardiovascular disease.
FUNDING:
Taiwan Department of Health Clinical Trial and Research Center of Excellence and National Health Research Institutes.

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By Team FPS – June 7, 2012

Blue Light, Cytochrome Oxidase, and Eye Injury

Also see:
Glucocorticoids, Cytochrome Oxidase, and Metabolism
Fat Deficient Animals – Activity of Cytochrome Oxidase
Light is Right
10 Tips for Better Sleep Quality
Using Sunlight to Sustain Life
Red Light Improves Mental Function
Light as Medicine? Researchers explain how
Red Light and Near-Infrared Radiation: Powerful Healing Tools You’ve Never Heard of
Get a “Chicken Light” and Amp Up Your Energy!
The Therapeutic Effects of Red and Near-Infrared Light (2015)
The Therapeutic Effects of Red and Near-Infrared Light (2017)
The Benefits of Near Infrared Light
MECHANISMS OF LOW LEVEL LIGHT THERAPY
The Lowdown on Blue Light: Good vs. Bad, and Its Connection to AMD
Light exposure and kids’ weight: Is there a link?

Article:
Blue light has a dark side
Smartphone overuse may ‘damage’ eyes, say opticians
Digital eye strain worse for multitaskers, survey finds

Videos:
Eye Damage from Blue Light

Quote by Ray Peat, PhD:
“By the 1960s, several studies had been published showing the inhibition of respiratory enzymes by blue light, and their activation by red light.”

“Old observations such as Warburg’s, that visible light can restore the activity of the “respiratory pigments,” showed without doubt that visible light is biochemically active. By the 1960s, several studies had been published showing the inhibition of respiratory enzymes by blue light, and their activation by red light. The problem to be explained is why the science culture simply couldn’t accept crucial facts of that sort.”

“Red and orange wavelengths penetrate tissue very effectively, because of their tissues because of their weaker absorption of water, allowing them to react with pigments in the cell, such as cytochrome oxidase, which is activated (or re-activated) by red light, increasing production of ATP. This effect counteracts the toxic effects of ultraviolet light, but there are probably other mechanism involved in the many beneficial effects of red light.”

“Blue light is now known to be toxic to the eye, by activating the oxidation of polyunsaturated fatty acids; it has been known to be toxic to various cells, including plant cells, for more than 50 years. In the eye, blue light creates free radicals in melanin, which catalyze the oxidations.”

“Cytochrome oxidase is one of the enzymes damaged by stress and by blue light, and activated or restored by red light, thyroid, and progesterone. It’s a copper enzyme, so it’s likely to be damaged by excess iron. It is most active when it is associated with a mitochondrial lipid, cardiolipin, that contains saturated palmitic acid; the substitution of polyunsaturated fats lowers its activity. Mitochonrial function in general is poisoned by the unsaturated fats, especially arachidonic acid and DHA.”

“Red light is protective, blue light (or u.v.) is harmful, so wearing orange lenses would be helpful. Progesterone and pregnenolone, by reducing the stress reactions, should be helpful–in the eye diseases of infancy and old age, as they are in the respiratory distress syndromes.”

Graefes Arch Clin Exp Ophthalmol. 1993 Jul;231(7):416-23.
Inhibition of cytochrome oxidase and blue-light damage in rat retina.
Chen E.
The activity of cytochrome oxidase, outer nuclear layer thickness, and edema were quantitatively evaluated in the blue-light exposed rat retina. Dark-adapted or cyclic-light reared rats were exposed to blue light with a retinal dose of 380 kJ/m2. Immediately, 1, 2, and 3 day(s) after exposure, the retinas of six rats from each adaptation group were examined. There was no difference between the dark-adapted and cyclic-light reared rats. Immediately after light exposure, cytochrome oxidase activity decreased. The activity in the inner segments remained low at day 1, while severe edema was observed in the inner and outer segments. The outer nuclear layer thickness decreased 1-3 days after exposure. The blue-light exposure inhibited cytochrome oxidase activity and caused retinal injury. Similarity of the injury process in the dark-adapted and cyclic-light reared retinas suggests that rhodopsin was not involved. The inhibition of cytochrome oxidase could be a cause of retinal damage.

Acta Ophthalmol Suppl. 1993;(208):1-50.
Inhibition of enzymes by short-wave optical radiation and its effect on the retina.
Chen E.
Exposure to short-wave optical radiation is a potential hazard for vision. In the present study, blue-light damage is studied in rat retina. It was hypothesized that the absorption of blue light by cytochrome oxidase in rat retina inhibits this enzyme, and may reduce the retinal oxidative metabolism. Irreversible inhibition of the oxidative metabolism may decrease the activity of the Na/K-ATPase, hence redistribute ions, increase intracellular osmotic pressure and cause cellular edema. Severe retinal edema may be the cause of retinal degeneration…Blue light inhibited cytochrome oxidase at a retinal dose of about 110 kJ/m2. This inhibition was reversible, and is probably related to the light regulation of retinal metabolism. At a retinal dose of about 380 kJ/m2, the inhibition of cytochrome oxidase was followed consecutively by a probable redistribution of chlorine and potassium in the inner and outer segments, damage to the mitochondria in the inner segments, edema in the inner and outer segments, and progressive degeneration of photoreceptor cells. Dark adaptation did not increase the blue-light retinal injury. These findings support the hypothesis that inhibition of cytochrome oxidase is one of the causes of blue-light retinal damage. The alteration of enzyme kinetics after in vitro exposure to short-wave optical radiation was estimated using lactate dehydrogenase as a model. The ultraviolet-radiation exposure inhibited lactate dehydrogenase with a significant decrease in maximal velocity, while Michaelis constant remained unchanged.

Curr Eye Res. 1992 Sep;11(9):825-31.
Cytochrome oxidase activity in rat retina after exposure to 404 nm blue light.
Chen E, Söderberg PG, Lindström B.
Cytochrome oxidase (CYO), a key enzyme in the respiratory chain, was observed as an indicator of retinal metabolism after an in vivo blue light exposure. Thirty Sprague-Dawley rats were exposed to optic radiation of 404 nm with a retinal dose of 110kJ/m2. Immediately after exposure, the CYO activity in the pigment epithelium, in the outer and inner segments of photoreceptors, and in the outer plexiform layer of the exposed retina, was reduced to one-third-to-half of the control level. However, there was an increase in CYO activity in the exposed retina one day after exposure. One week after exposure, the CYO activity in the inner segment and the outer plexiform layer was higher, while the activity in the other two layers was lower, than that at one day, although still higher than in the control. Two weeks after exposure, the CYO activity in the four retinal layers returned to the level of the control retina, as did the activity four weeks after. After exposure, no ophthalmoscopically visible retinal change and no light-microscopically evident morphological alterations were found. There was no retinal edema or loss of photoreceptor cells. The observed alteration in CYO activity after blue light exposure may represent an inhibition of retinal metabolism. The inhibition was reversible. If this compensation mechanism is overwhelmed, retinal damage may occur.

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By Team FPS – June 6, 2012

Estrogen and Liver Toxicity

Also see:
Estrogen, Endotoxin, and Alcohol-Induced Liver Injury
Alcohol Consumption – Estrogen and Progesterone In Women
How does estrogen enhance endotoxin toxicity? Let me count the ways.
PUFA and Liver Toxicity; Protection by Saturated Fats
Endotoxin: Poisoning from the Inside Out

“Many things in our environment are increasing the incidence of certain kinds of liver disease. The liver processes things that are ingested or that enter the blood stream after being inhaled or absorbed through the skin, so in a toxic environment it is susceptible to injury. If deprived of good nutrition or adequate thyroid hormone it is especially sensitive to toxins. The body’s own estrogen is a burden on the liver, causing women’s livers to be on average slower than men’s in processing environmental chemicals.

Almost any kind of toxin causes the liver to be less efficient at excreting other substances, including hormones. In malnutrition, sickness, and in aging, there is a tendency for higher levels of estrogen to remain circulating in the blood.” -Ray Peat, PhD

J Korean Med Sci. 1999 Jun;14(3):277-85.
The metabolic effects of estriol in female rat liver.
Yang JM, Kim SS, Kim JI, Ahn BM, Choi SW, Kim JK, Lee CD, Chung KW, Sun HS, Park DH, Thurman RG.
The effects of estriol on oxygen uptake, glucose release, lactate and pyruvate production, beta-hydroxybutyrate and acetoacetate production in perfused rat liver as well as, carbon uptake in rat liver and intracellular calcium in isolated Kupffer cells were investigated. Basal oxygen consumption of perfused liver increased significantly in estriol or ethanol-treated rats. But these increased effects were blocked by gadolinium chloride pretreatment. In a metabolic study, pretreatment with estriol resulted in a decrease in glucose production and in glycolysis while an increase in ketogenesis. A more oxidized redox state of the mitochondria was indicated by increased ratios of perfusate [lactate]/[pyruvate] and decreased ratios of perfusate [beta-hydroxybutyrate]/[acetoacetate]. Carbon uptake of Kupffer-cell increased significantly in estriol-treated rats. But these increased uptake were not shown in rats pre-treated by gadolinium chloride blocking phagocytosis. In isolated Kupffer cells from estriol-treated rats, intracellular calcium was more significantly increased after addition of lipopolysaccharide (LPS) than in controls. These findings suggest that the metabolic effects of estriol (two mg per 100 mg body wt) can be summarized to be highly toxic in rat liver, and these findings suggest that oral administration of estrogens may induce hepatic dysfunctions and play a role in the development of liver disease.

Estrogen makes the toxic-mediator-producing cells in the liver (Kupffer cells) hypersensitive to LPS–15 times more sensitive than normal (Ikejima, et al., 1998). One way estrogen increases the toxicity of endotoxin is probably by making the intestine more permeable (Enomoto, et al., 1999). -Ray Peat, PhD

Am J Physiol. 1998 Apr;274(4 Pt 1):G669-76.
Estrogen increases sensitivity of hepatic Kupffer cells to endotoxin.
Ikejima K, Enomoto N, Iimuro Y, Ikejima A, Fang D, Xu J, Forman DT, Brenner DA, Thurman RG.
The relationship among gender, lipopolysaccharide (LPS), and liver disease is complex. Accordingly, the effect of estrogen on activation of Kupffer cells by endotoxin was studied. All rats given estrogen intraperitoneally 24 h before an injection of a sublethal dose of LPS (5 mg/kg) died within 24 h, whereas none of the control rats died. Mortality was prevented totally by pretreatment with gadolinium chloride, a Kupffer cell toxicant. Peak serum tumor necrosis factor-alpha (TNF-alpha) values as well as TNF-alpha mRNA in the liver after LPS were twice as high in the estrogen-treated group as in the untreated controls. Plasma nitrite levels and inducible nitric oxide synthase in the liver were also elevated significantly in estrogen-treated rats 6 h after LPS. Furthermore, Kupffer cells isolated from estrogen-treated rats produced about twice as much TNF-alpha and nitrite as controls did in response to LPS. In addition, Kupffer cells from estrogen-treated rats required 15-fold lower amounts of LPS to increase intracellular Ca2+ than controls did, and Kupffer cells from estrogen-treated animals expressed more CD14, the receptor for LPS/LPS binding protein, than controls. Moreover, estrogen treatment increased LPS binding protein mRNA dramatically in liver in 6-24 h. It is concluded that estrogen treatment in vivo sensitizes Kupffer cells to LPS, leading to increased toxic mediator production by the liver.

Am J Physiol. 1999 Sep;277(3 Pt 1):G671-7.
Estriol sensitizes rat Kupffer cells via gut-derived endotoxin.
Enomoto N, Yamashina S, Schemmer P, Rivera CA, Bradford BU, Enomoto A, Brenner DA, Thurman RG.
The relationship between gender and alcohol-induced liver disease is complex; however, endotoxin is most likely involved. Recently, it was reported that estriol activated Kupffer cells by upregulation of the endotoxin receptor CD14. Therefore, the purpose of this work was to study how estriol sensitizes Kupffer cells. Rats were given estriol (20 mg/kg ip), and Kupffer cells were isolated 24 h later. After addition of lipopolysaccharide (LPS), intracellular Ca2+ concentration was measured using a microspectrofluorometer with the fluorescent indicator fura 2, and tumor necrosis factor-alpha was measured by ELISA. CD14 was evaluated by Western analysis. One-half of the rats given estriol intraperitoneally 24 h before an injection of a sublethal dose of LPS (5 mg/kg) died within 24 h, whereas none of the control rats died. Mortality was prevented totally by sterilization of the gut with antibiotics. A similar pattern was obtained with liver histology and serum transaminases. Translocation of horseradish peroxidase was increased about threefold in gut segments by treatment with estriol. This increase was not altered by treatment with nonabsorbable antibiotics. On the other hand, endotoxin levels were increased to 60-70 pg/ml in plasma of rats treated with estriol. As expected, this increase was prevented (<20 pg/ml) by antibiotics. In isolated Kupffer cells, LPS-induced increases in intracellular Ca2+ concentration, tumor necrosis factor-alpha production, and CD14 were increased, as previously reported. All these phenomena were blocked by antibiotics. Therefore, it is concluded that estriol treatment in vivo sensitizes Kupffer cells to LPS via mechanisms dependent on increases in CD14. This is most likely due to elevated portal blood endotoxin caused by increased gut permeability.

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By Team FPS – June 6, 2012

Estrogen Related to Loss of Fat Free Mass with Aging

Also See:
Fat Tissue and Aging – Increased Estrogen
Estrogen Levels Increase with Age
Resistance Training Limits Age-Related Muscle & Strength Loss

A recent study (Toth, et al., 2000) shows that, at least in women, estrogen is closely associated with the general loss of fat-free tissue with aging. This shows a close association between the generalized atrophy of aging and the amount of estrogen in the tissues. -Ray Peat, PhD

“Muscle physiologists and endocrine physiologists know that fatigue, stress and excess estrogen can cause the tissues to swell hugely, increasing their weight and water content without increasing their protein content.

As soon as cheap synthetic estrogens, such as DES, became available in the 1940s, their use in animals was promoted because it was clear that they caused massive water retention. Women who suffer from hyperestrogenism always have a problem with water retention, but they have never been known to suffer from over-developed skeletal muscles. In fact, in humans of both sexes, an excess of estrogen has been commonly associated with sarcopenia, muscular dystrophy, and atrophy of the skeletal muscles. Similar observations have been made in a variety of animals. Meat scientists are the only people I know of who have ever referred to estrogen as an anabolic steroid, in the sense of “building muscle.” -Ray Peat, PhD

J Clin Endocrinol Metab. 2000 Apr;85(4):1382-7.
Regulation of protein metabolism in middle-aged, premenopausal women: roles of adiposity and estradiol.
Toth MJ, Tchernof A, Rosen CJ, Matthews DE, Poehlman ET.
The age-related loss of fat-free mass (FFM) is accelerated in women during the middle-age years and continues at an increased rate throughout the postmenopausal period. Because protein is the primary structural component of fat-free tissue, changes in FFM are largely due to alterations in protein metabolism. Knowledge of the hormonal and physiological correlates of protein metabolism in middle-aged women, therefore, has important implications for understanding the mechanisms underlying changes in FFM. We measured leucine kinetics (expressed relative to FFM: micromol/kg FFM/h) in 46 middle-aged, premenopausal women (mean +/- SD, 47 +/- 3 yr) after an overnight fast (i.e. basal) and during euglycemic hyperinsulinemia (40 mU/m2/min) using a 5.5-h infusion of [1-13C]leucine. Additionally, we measured insulin-stimulated glucose disposal by euglycemic hyperinsulinemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution by computed tomography, and hormone levels by RIA as possible correlates of protein metabolism. Under basal conditions, stepwise regression analysis showed that leucine appearance (i.e. protein breakdown) was related to percent body fat and serum estradiol (r2 = 40%; P < 0.01), and leucine oxidation was related to serum estradiol and percent body fat (r2 = 26%; P < 0.05). Under euglycemic hyperinsulinemic conditions, no variables correlated with the percent change in leucine appearance. The percent change in leucine oxidation was related to intraabdominal adipose tissue area and glucose disposal rate (r2 = 48%; P < 0.01). Correlates and r2 values for nonoxidative leucine disposal (i.e. protein synthesis) under basal and euglycemic hyperinsulinemic conditions were similar to those observed for leucine appearance. From these results, we conclude that adiposity and/or serum estradiol may contribute to the regulation of protein metabolism and FFM in middle-aged, premenopausal women.

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By Team FPS – June 6, 2012

Carrageenan: A pseudo-latex allergy

Also see:
Carrageenan, Inflammation, Cancer, Immunity
Plant Toxins in Response to Stress
Doubts surface about safety of common food additive, carrageenan
Carrageenan: How a “Natural” Food Additive is Making Us Sick

J Allergy Clin Immunol. 1995 May;95(5 Pt 1):933-6.
Anaphylaxis to carrageenan: a pseudo-latex allergy.
Tarlo SM, Dolovich J, Listgarten C.
Source
Toronto Hospital, Western Division, Ontario, Canada.
Abstract
BACKGROUND:
Anaphylactic reactions during a barium enema have been attributed to allergy to latex on the barium enema device. The observation of anaphylaxis during barium enema without latex exposure or latex allergy led to the performance of an allergy skin test to the barium enema solution.
METHODS:
Individual components of the barium enema solution were obtained for double-blind skin testing. A RAST to identify specific IgE antibodies to the skin test active agent was established.
RESULTS:
Carrageenan, a component of the barium enema solution, produced positive reactions to allergy skin test and RAST. Gastrointestinal symptoms for which the patient was being investigated by the barium enema subsequently disappeared with a diet free of carrageenan.
CONCLUSIONS:
Carrageenan is a previously unreported cause of anaphylaxis during barium enema. It is an allergen widely distributed in common foods and potentially could account for some symptoms related to milk products or baby formula.

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By Team FPS – June 4, 2012