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Buying Under the Influence (of Testosterone)

Buying Under the Influence (of Testosterone)

Summary: Researchers say men with higher testosterone levels have a greater preference for goods that are considered to be luxurious status symbols.

Source: CalTech.

Some men, it seems, can’t get enough of luxury goods like European sports cars or designer jeans. Now, scientists have figured out why: testosterone.

A new study shows that testosterone has a measurable effect on a man’s preference for brands that are considered to be status symbols. For instance, a man with a higher level of testosterone in his body will be more likely than a man with lower testosterone levels to prefer a pair of Calvin Klein jeans over a pair of Levi’s.

That makes sense, says Caltech’s Colin Camerer, one of the authors of the study that appears in the July 3 edition of Nature Communications, because one of the primary functions of testosterone is to generate both status-seeking and status-protecting behaviors.

“In the animal kingdom, testosterone promotes aggression, but the aggression is in service of status,” says Camerer, the Robert Kirby Professor of Behavioral Economics and the T&C Chen Center for Social and Decision Neuroscience Leadership Chair. “A lot of human behaviors are repurposed behaviors seen in our primate relatives. So, here, we’re replacing physical aggression with a sort of ‘consumer’ aggression.”

The study—conducted by researchers from Caltech, the Wharton School of the University of Pennsylvania, University of Western Ontario, and ZRT Laboratory—gets to the biological heart of what we call conspicuous consumption, the human practice of acquiring and showing off luxury goods and services to increase one’s social status. Camerer likens the costs of this behavior to the cost and weight of the elaborate tails carried around by male peacocks.

“If it didn’t need to attract mates, a peacock would be better off without its tail. It would be easier for the peacock to escape from predators and easier for it to find food if it wasn’t carrying that tail around,” he says. “In biology, that’s known as costly signaling. A human male would probably be better off not spending $300,000 on a car but, by buying that car, he’s showing people that he’s wealthy enough that he can.”

The study included 243 male volunteers between the ages of 18 and 55 who were randomly selected to receive a dose of testosterone gel or placebo gel that would absorb through their skin. They were sent home and asked to return to the lab about four hours later, when testosterone levels in their blood would be near peak. Upon returning, they participated in tasks designed to gauge their preferences for different types of goods.

The first task presented participants with a 10-point scale that had a brand associated with high social status at one end and a brand with lower social status but otherwise equivalent quality at the other end. They were asked to move a slider toward the brand they preferred with the slider’s proximity to the brand indicating how strong their preference was.

The data the researchers collected during this task showed that the men who received a dose of testosterone had a stronger preference for the luxury brands than did the men who received the placebo.

The second task was designed to tease apart testosterone’s effect on the desire for luxury good from other potential effects, like an increased desire for high-quality goods or for goods that evoked a sense of power.

a red sports car

The task presented the study participants with a series of ads for consumer goods such as a car, a pair of sunglasses, or a coffee machine. The participants were randomly presented with one of three versions of an advertisement for each item, with each version of the ad emphasizing either the item’s quality, luxuriousness, or power. After reviewing the ad, they were asked to rate their attitude toward that item on a scale of 1–10.

The data from this task—as with the first task—showed that men who received a dose of testosterone had a stronger preference for luxury goods than men who received the placebo. There was no corresponding increase in preference for goods that were advertised as powerful or higher in quality.

“In our closest animal kin, males spend a lot of time and energy fighting to establish dominance. We do, too, but our weapons are what we wear, drive, and live in rather than claws, fists, and muscles,” Camerer says.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Funding and support for the study was provided by INSEAD, the MacArthur Foundation, Ivey Business School, the International Foundation for Research in Experimental Economics, and the Russell Sage Foundation.

Source: Emily Velasco – CalTech
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Single-dose testosterone administration increases men’s preference for status goods” by G. Nave, A. Nadler, D. Dubois, D. Zava, C. Camerer & H. Plassmann in Nature Communications. Published July 3 2018.
doi:10.1038/s41467-018-04923-0

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Abstract

Single-dose testosterone administration increases men’s preference for status goods

In modern human cultures where social hierarchies are ubiquitous, people typically signal their hierarchical position through consumption of positional goods—goods that convey one’s social position, such as luxury products. Building on animal research and early correlational human studies linking the sex steroid hormone testosterone with hierarchical social interactions, we investigate the influence of testosterone on men’s preferences for positional goods. Using a placebo-controlled experiment (N = 243) to measure individuals’ desire for status brands and products, we find that administering testosterone increases men’s preference for status brands, compared to brands of similar perceived quality but lower perceived status. Furthermore, testosterone increases positive attitudes toward positional goods when they are described as status-enhancing, but not when they are described as power-enhancing or high in quality. Our results provide novel causal evidence for the biological roots of men’s preferences for status, bridging decades of animal behavioral studies with contemporary consumer research.

Maternal vaginal microbiota exhibited increased stress hormones

 

How Shift Work Disrupts Metabolism

How Shift Work Disrupts Metabolism

Summary: Researchers report metabolic disruptions often seen in shift workers are not influenced by the brain’s circadian rhythm, but by peripheral oscillators in the liver, gut and pancreas.

Source: Washington State University.

Working night shifts or other nonstandard work schedules increases your risk of becoming obese and developing diabetes and other metabolic disorders, which ultimately also raises your risk of heart disease, stroke and cancer.

Exactly why this happens has been unclear, but a new study conducted at Washington State University (WSU) has brought scientists closer to finding the answer.

Published in this week’s online edition of the Proceedings of the National Academy of Sciences, the study dispels the belief that the metabolic disruption in shift workers is driven primarily by the brain’s master clock, which normally keeps our bodies on a day-night cycle and uses light cues to synchronize the rhythms of the body’s organs and tissues. Instead, the study revealed that separate biological clocks (so-called peripheral oscillators) in the liver, gut and pancreas have a mind of their own.

Working with colleagues at the University of Surrey, the WSU team collected blood samples from healthy volunteers who had just completed either a simulated day shift schedule or a simulated night shift schedule. The investigators analyzed the blood samples for metabolites–products of chemical reactions involved in digestion, such as the breakdown and oxidization of food molecules, as well as in other metabolic processes in cells and organs. They found that, following the night shift schedule, 24-hour rhythms in metabolites related to the digestive system had shifted by a full 12 hours, even though the master biological clock in participants’ brains had only moved by about 2 hours.

Biological clocks in digestive organs

“No one knew that biological clocks in people’s digestive organs are so profoundly and quickly changed by shift work schedules, even though the brain’s master clock barely adapts to such schedules,” said co-senior author Hans Van Dongen, director of the WSU Sleep and Performance Research Center and a professor in the Elson S. Floyd College of Medicine. “As a result, some biological signals in shift workers’ bodies are saying it’s day while other signals are saying it’s night, which causes disruption of metabolism.”

Van Dongen said the next step is to find out whether the shifted metabolite rhythms are driven by the shift workers’ altered sleep/wake schedules, the changed timing of their food intake, or both. Once that is known, scientists could try to pinpoint the underlying cellular and/or hormonal processes, which would support the development of new treatments to resynchronize shift workers’ brain and body clocks to prevent negative long-term health consequences.

Long-term health consequences

The research team’s work may also have implications for the study of other chronic diseases shift workers are more susceptible to, including chronic kidney disease and breast, prostate and skin cancer.

“We believe ours is the first study to suggest a mechanism for the connection between shift work and chronic kidney disease,” said co-senior author Shobhan Gaddameedhi, an assistant professor in the WSU College of Pharmacy and Pharmaceutical Sciences. He noted that the simulated night shift group had altered rhythms in two metabolites commonly associated with chronic kidney disease — tryptophan and kynurenine.

bed sheets

However, as a cancer biologist, Gaddameedhi first and foremost wants to unravel the link between shift work and cancer.

“It’s possible that changes in the metabolism of shift workers are associated with altered activity of cellular processes that may be involved in cancer development later in life,” Gaddameedhi said. “Once we understand those cellular processes, we could potentially identify the genes involved and use that knowledge to find ways to prevent cancer in shift workers.”

Metabolomics Used to Study Rhythms

The study included 14 participants who each spent seven days inside the sleep laboratory at the WSU Health Sciences Spokane campus. First, half of them completed a three-day simulated night shift schedule, while the rest were on a three-day simulated day shift schedule. Then, after completing their simulated shifts, all participants were kept in a constant routine protocol used to study humans’ internally generated biological rhythms independent of any external influences.

During this protocol, they were kept awake for 24 hours in a semireclined posture. They received identical snacks every hour and were kept under constant light exposure and room temperature. Every three hours a blood sample was drawn.

The blood samples were analyzed at the University of Surrey’s Metabolomics Core Facility for 132 different metabolites related to metabolism and the digestive system.

“Twenty-seven metabolites followed a 24-hour rhythm during both the simulated night and day shift schedules,” said first author Debra Skene, professor of neuroendocrinology at the University of Surrey. “Of these, 24 displayed a dramatic 12-hour shift in rhythm following the simulated night shift schedule, which was not observed following the day shift schedule. This indicated that just three days of being on a night shift schedule has the potential to disrupt metabolism. Pinpointing the disrupted metabolic pathways will help unravel the mechanisms underlying shift work and metabolic disorders.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

In addition to Skene, Van Dongen, and Gaddameedhi, co-authors include Elena Skornyakov, Rajendra Gajula, Brieann Satterfield, and Kenneth Porter of WSU and Namrata Chowdhury and Benita Middleton of the University of Surrey.

Funding: Support for the study came from internal funding from the WSU College of Pharmacy and Pharmaceutical Sciences, as well as grants awarded to WSU by the Congressionally Directed Medical Research Program and National Institutes of Health and to the University of Surrey by the UK Biotechnology and Biological Sciences Research Council and the European Union’s Seventh Framework Programme.

Source: Hans Van Dongen – Washington State University
Publisher: Organized by NeuroscienceNews.com.

Link Between Autoimmune Disorder and Psychosis Confirmed

Link Between Autoimmune Disorder and Psychosis Confirmed

Summary: A new study confirms a link between a number of autoimmune diseases and an increased risk of developing psychosis.
Source: The Conversation.

People with autoimmune disorders, a collection of diseases where the body’s immune system attacks its own cells, are more likely to have psychosis, according to our latest research.

Previous research found that rates of rheumatoid arthritis were lower in people with psychosis than would be expected in the general population. But later studies showed that other autoimmune disorders, such as coeliac disease and autoimmune thyroid disorders, were more common in people with psychosis. This led scientists to the view that there is a connection between autoimmune disorders and psychosis. But conflicting findings meant that it was difficult to reach any conclusions about the relationship.

Given the uncertainty about the relationship between these disorders and psychosis, and growing interest in this area, we decided to review the research and conduct a meta-analysis – a method in which data from several studies are combined and analysed together to give a more statistically robust result than individual studies can provide.

Our study, which is published in Biological Psychiatry, included 30 relevant studies, and contained data on 25m people.

What we found

We focused on autoimmune disorders that affect the peripheral system, such as type 1 diabetes, as we were particularly interested in whether autoimmune disorders that target the body, as opposed to the brain, could still influence the development of psychosis.

For our main analysis, we combined data from all non-neurological autoimmune disorders, except for rheumatoid arthritis (given the well-established negative association reported with psychosis) and found that, overall, people with any autoimmune disorder were 40% more likely to have a psychotic disorder, such as schizophrenia.

For our secondary analysis, we examined individual autoimmune disorders. We found the likelihood of having psychosis was higher for pernicious anaemia, pemphigoid (a disease characterised by skin blisters), psoriasis, coeliac disease and Graves’ disease (the disease suffered by Marty Feldman that causes protrusion of the eyeballs). But it was lower for rheumatoid arthritis and ankylosing spondylitis (a type of arthritis that mainly affects the spine), suggesting that these disorders are protective.

Looking for causes

There are a range of possible mechanisms that might underlie the relationships we found. Given that people with psychosis have also been found to show higher levels of inflammatory markers in the blood than healthy people, and that inflammation is a core feature of autoimmune disorders, inflammation is a likely candidate.

But rheumatoid arthritis and ankylosing spondylitis are also characterised by higher levels of inflammation, so this would not explain the negative relationships we found with these disorders. Although all autoimmune disorders activate the body’s immune system, the exact response differs depending on the disorder. This might go some way to explaining why we found different relationships for individual autoimmune disorders, and suggests that inflammation cannot be the only mechanism.

It is possible that there might be a genetic link between autoimmune disorders and psychosis. In fact, research has recently shown that variations within specific genes are associated with both schizophrenia and rheumatoid arthritis. That is, people with one variation of the gene are at risk for schizophrenia, while people with the other variation are at risk for rheumatoid arthritis. This might explain why rheumatoid arthritis appears to be protective for psychosis.

Newly discovered antibodies (part of the immune system’s armoury) that go rogue and mistakenly attack brain cells might also explain the link. These sorts of antibodies are thought to cause psychotic symptoms, such as paranoia and hallucinations, in some people.

Although our study cannot tell us why autoimmune disorders and psychosis occur together more commonly than we would expect, it provides stronger evidence that a relationship does exist.

immune system diagram

Our group is involved in further research to help us better understand the mechanisms that might underlie this complex relationship.

Early intervention

So what is the real-world application of these findings? Although the risk of psychosis is only slightly increased for people with autoimmune disorders, our findings suggest that perhaps doctors ought to monitor people with certain autoimmune disorders for early signs of psychosis – especially pernicious anaemia, Graves’ disease and pemphigoid, which showed the most consistent relationships with psychosis. This is important because early intervention has been shown to improve long-term outcomes for people in the initial stages of a psychotic disorder.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Alexis E. Cullen is funded by a Sir Henry Wellcome Postdoctoral Fellowship (107395/Z/15/Z).

Source: Alexis E Cullen – The Conversation
Publisher: Organized by NeuroscienceNews.com.

Children who are habitually barefoot have better balance and jumping skills

 

Medically driven food prohibitions

Medically driven food prohibitions

(compiled from NORD [])

Disease/Syndrome Causative Food Cause Comment
Disaccharide intolerance Sucrose, dextrins Autosomal recessive trait characterized by the deficiency or absence of enzymes sucrase and isomaltase in the intestine. Attacks characterized by bloating and diarrhea.
Favism Broadbean (Vicia fava) X-linked recessive trait resulting in low amounts of glucose-P-dehydrogenase. Several subtypes known. Hemolytic anemia may result from consumption of offending foods.
Galactosemia Galactose and lactose (dairy products) Autosomal recessive trait with low levels of any one of three enzymes directly responsible for galactose metabolism. High levels of galactose in the blood results in hepatomegaly, cirrhosis, and renal failure. Infant mortality is ~75%.
Gluten intolerance Wheat, barley, gluten containing foods Autoimmune disease Sensitivity to storage protein (gliadin) in some grains.
Lactose intolerance Dairy products Inborn error of metabolism—low or no lactase enzyme in the intestine. Lactase is required to cleave lactose (a disaccharide of galactose and glucose). Bloating and diarrhea may develop.
Ornithine transcarbamylase deficiency Dietary nitrogen (primarily meat) X-linked recessive disorder resulting in low production of hepatic ornithine transcarbamylase interrupting the urea cycle and leading to accumulation of ammonia. Although usually first seen in neonates, there may be an adult onset.
Citrullinemia is another genetic disease affecting the urea cycle.
Phenylketonuria (PKU disease) Phenylalanine in foods Autosomal recessive trait characterized by inadequate hepatic phenylalanine hydroxylase. Leads to accumulation of phenylpyruvate which may accumulate in the brain and lead to seizures, mental retardation, etc.Products containing phenylalaine must be labeled.
Refractory sprue Wheat, barley and rye Autoimmune disorder triggered by gliadin, a gluten storage protein. Unlike common celiac sprue, adherence to a gluten-free diet may not cause symptoms to abate.
Trimethylaminuria Fish Autosomal recessive resulting in low production of flavin containing monoxygenase enzyme 3 (FMO3). Fish odor syndrome. Failure to breakdown trimethylamine, a build of which results in a fish odor.
Very long chain Acyl CoA dehydrogenase deficiency (LCAD) Very long chain fatty acids Autosomal recessive trait resulting from a mutation in the HADHA gene. Prevents mitochondrial metabolism of very long chain fatty acids.

Other medically driven prohibitions include food allergies, the most common of which are to milk, egg, fish, crustacean shellfish, tree nuts, wheat, peanuts and soybeans which account for 90% of all food allergies in the US. The Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA), effective January 1, 2006, requires labeling of any product containing these ingredients or a protein derived from one of these offending foods or incidental additives or flavors derived therefrom. Exceptions are limited to any highly refined oil derived from a major food allergen (e.g., peanut or soybean oil) or any food ingredient exempt from labeling under a petition or notification process specified in the law [].

There are also a number of food-drug interactions, the consumption of one interfering with the metabolism of the other, which may result in an enhanced or abated effect of the drug (Table 2).

Food drug interactions

Used with permission from Kotsonis and Burdock []

Enzyme or Transporter Food Drug
CYP1A2 Caffeine, theophylline, grapefruit juice (naringen and furanocourmarins bergmottin and dihydroxybergamotin), grape juice, cruciferous vegetables, apiaceous vegetables, cooked meat Clozapine, fluvoxamine, imipramine
CYP2E1 Watercress and possibly other isothiocyanate-containing cruciferous vegetables; polyunsaturated fatty acids (corn oil, menhaden oil) Ethanol, halothane, enflurane
CYP3A4 Grapefruit, orange juice, red wine, possibly other polyphenol-containing substances, St. Johns wort, garlic Ketoconazole, cyclosporine, erythromycin, protease inhibitors, HMG-CoA reductase inhibitors
UGT and GST Brussels sprouts, cabbage, watercress, broccoli Acetaminophen, oxazepam, morphine, ibuprofen
P-glycopeptide and OATP Vegetables, fruit juice, St. Johns wort Digoxin, cyclosporine, parvastatin

Toxin Incorporation during Growth, Storage or Processing

Environmental contaminants

Selenium in grain

Selenium (Se) enters the food chain via plant and microorganism conversion of inorganic selenium to organically bound forms []. Selenium toxicity (i.e., selenosis), caused by excessive selenium intake, has occurred on a large scale in seleniferous regions in China as the result of increased consumption of selenium-containing foods (approximate daily intake of 3–6.5 mg Se/day) []. The most common symptoms of selenosis are loss of hair, deformity, and loss of nails. Other reported symptoms include increased blood selenium levels, diarrhea, fatigue, a garlic-like odor of the breath and bodily secretions, irritability, peripheral neuropathy, and skin lesions []. Selenium intake levels that cause selenosis have not yet been well defined. Studies in China suggest that approximately 3–5 mg/day (0.05–0.08 mg/kg/day) will cause selenosis. Residents of seleniferous regions in South Dakota who consumed approximately 700 µg selenium/day (0.01 mg/kg/day) showed no symptoms of selenosis. The EPA has proposed an oral reference dose (RfD) of 0.005 mg/kg bw/day, or 350 µg/day [].

Methyl mercury in seafood

Exposure to elemental mercury is relatively rare, although was once an occupational disease of hat manufacturers as elemental mercury was used for the curing of animal pelts. Inhalation of the mercury fumes led to mental deterioration and subsequently named “mad hatter syndrome” [].

Of interest to food toxicology, is the methyl derivative, methyl mercury, formed by bacterial action in an aquatic environment from anthropogenic and natural sources of elemental mercury. Anthropogenic sources include burning of coal (which contains mercury), chloralkali process and other sources of elemental mercury into aquatic environments. In the case of Minamata, Japan, there was a direct discharge of methyl mercury into the environment.

Methyl mercury exposure may cause neurological paresthesias, ataxia, dysarthria, hearing defects and death. Developmental delays have been documented in children borne of mothers exposed to methyl mercury []. Other than direct exposure to methyl mercury, exposure usually comes about as the result of methyl mercury becoming incorporated into the food chain, moving up as each predator consumes the smaller and less fortunate animal.

Near the peak of the food chain, methyl mercury becomes concentrated in fish including, bonito (Sarda spp.), halibut (Hippoglossus spp.), mackerel (Scomberomorus spp.), marlin (Makaira spp.), shark (all species), swordfish (Xiphias gladius), and bluefin tuna (Thunnus spp.). The selection of these species was based on historical data on levels of methyl mercury found in fish consumed in the U.S. The selection was also based on an FDA action level of 1.0 ppm in the edible portion of fish []. However, the allowable level of mercury depends on whether the mercury was “added”; that is, did the presence of mercury arise from an anthropogenic source (i.e., was the fish caught in an area known for mercury discharge), or was not added and the result of mercury naturally present in the environment [].

Naturally formed substances

β-Thujone

Thujone, a monoterpene ketone, is the primary constituent of essential oils derived from a variety of plants, including sage (Salvia officinalis), clary (Salvia sclarea), tansy (Tanacetum vulgare), wormwood (Artemisia spp. and white cedar (Thuja occidentalis L.) []. Essential oils from these plants are used in herbal medicines, as flavorings in alcoholic drinks and fragrances throughout the world. Thujone is potentially toxic and the presence of alpha- or beta-thujone in food and beverages is regulated by law in several countries. In the US, thujone as an isolated substance is banned as an ingredient to be added to food and many of the natural thujone-containing plant oils (e.g., wormwood, white cedar, oak moss (Evernia prunastri) and tansy) are used as flavorings in food under the condition that the finished food is thujone-free []. Absinthe (made from wormwood) contains significant levels of thujone and is available in Spain, Denmark and Portugal. Wormwood itself is a popular flavoring for vodka in Sweden, while vermouth, chartreuse, and Benedictine all contain small levels of thujone []. Sage oil is used to provide the characteristic flavor in sausages, meats, condiments and sauces, and contains approximately 20–30% thujone (alpha- and beta-) [,].

Both alpha- and beta-thujone act as noncompetitive blockers of the gamma-aminobutyric acid (GABA)-gated chloride channel []. The essential oils of sage, hyssop (Hyssopus officinalis L.), and cedar all contain thujone and have been cited to have caused central nervous system effects characterized by tonic-clonic or solely clonic convulsions []. Thujone is believed to be the toxic agent in absinthism, a syndrome produced by the chronic use of absinthe, made from the essence of wormwood. The syndrome is characterized by addiction, hyperexcitability and hallucinations. The debilitating illnesses suffered by Vincent Van Gogh and Henri de Toulouse-Lautrec have been linked to absinthism, while the toxicity of thujone was a major factor in banning absinthe in the early 1900s []. A published case report detailed a male subject that drank about 10 mL of essential oil of wormwood (believing it was absinthe) and became agitated, incoherent and disoriented, subsequently developing renal failure []. The no observable effect limit (NOEL) for convulsions in subchronic toxicity studies in female rats was 5 mg/kg bw/day []. Detoxification of thujone is thought to occur via CYP450-dependent oxidation and subsequent glucuronidation and excretion []. The FDA limits exposure to β-thujone from Artemisia spp., when used as a natural flavoring substance or natural substance used in conjunction with flavors (21 CFR 182.20).

Prussic acid in cherry, apple and peach pits

Prussic acid (also known as hydrocyanic acid, hydrogen cyanide, or cyanide) is formed when cyanogenic glycosides found in leaves, cherry, apple and peach pits, oak moss and other plant tissues are damaged and come into contact with beta-glycosidase or emulsion enzymes. The enzymes release the cyanide from the glycoside, and the cyanide prevents the body’s cells from utilizing oxygen, resulting in cellular necrosis and tissue damage. The mucous membranes and blood are bright red as they are oxygenated, but the cells in the tissues cannot utilize the oxygen. Clinical signs of prussic acid poisoning include rapid breathing, trembling, incoordination and in extreme cases, respiratory and/or cardiac arrest []. Many fruit trees contain prussic acid glycosides in the leaves and seeds, but only negligible levels are present in the fleshy parts of the fruit []. In the west African tropics, cassava is consumed as a dietary staple and inappropriate handling of the cassava prior to processing and consumption can result in a chronic form of cyanide poisoning termed “tropical ataxic neuropathy”, the result of demyelinization of the optic, auditory, and peripheral nerve tracts [].

Prussic acid as found in flavoring ingredients is limited to 25 ppm in cherry pits (Prunus avium L. or P. cerasus L.), cherry laurel leaves (Prunus laurocerasus L.), elder tree leaves (Sambucus nigra L.), and peach leaves (Prunus persica (L.) Batsch) (21 CFR 172.510); although the extract of bitter almond (Prunus amygdalus Batsch, Prunus armeniaca L., or Prunus persica (L.) Batsch) must be prussic acid free (21 CFR 182.20). There are no FDA regulations or guidelines restricting the presence of prussic acid in apple seed (Malus spp.), probably because extracts of these seeds have no economic value as flavor ingredients.

Hypericin in St. John’s wort

St. John’s wort (Hypericum perforatum; Figure 1) is an herbal thought to alleviate symptoms of depression, and standardized extracts of St. John’s wort are consumed typically in tablet or capsule form. The major active antidepressive constituents in St. John’s wort are thought to be hyperforin and hypericin [,]. The mechanism of action is not fully understood, but may involve inhibition of serotonin (5-HT) reuptake, similar to conventional antidepressive drugs. In this manner, hyperforin and hypericin taken in conjunction with other serotonin reuptake inhibitors may contribute to serotonin syndrome, a potentially life-threatening elevation of serotonin in the central nervous system. Hyperforin is also known to induce cytochrome P450 enzymes CYP3A4 and CYP2C9, which can lead to increased metabolism of certain drugs and decreased clinical response [].

Goitrogens (glucosinolates) in Brassica spp.

Certain raw foods have been found to contain substances that suppress the function of the thyroid gland by interfering with the uptake of iodine, an essential nutrient in growth, cognitive function, and hormonal balance. A lack of functional iodine is known to result in cognitive deficiencies (e.g., Cretinism). The decrease in iodine uptake causes the thyroid gland to enlarge, forming a goiter. Foods that have been identified as goitrogenic include spinach, cassava, peanuts, soybeans, strawberries, sweet potatoes, peaches, pears, and vegetables in the Brassica genus, which include broccoli, brussels sprouts, cabbage, canola, cauliflower, mustard greens, radishes, and rapeseed []. Goiter has also been attributed to the consumption of large quantities of uncooked kale or cabbage.

High temperatures (i.e., cooking) inactivate the goitrogenic substances, collectively termed glucosinolates. Cassava (Manihot esculenta) is an essential dietary source of energy in the tropics, but contains high levels of linamarin, a glucosinolate. Cassava must be properly processed-dried, soaked in water or baked to effectively reduce the linamarin content []. Glucosinolates are sulfur-containing substances that are metabolized in the body by thioglucosidase to form thiocyanate, isothiocyanate, nitriles and sulfur. Under certain conditions the isothiocyanates undergo cyclization to form goitrins, increasing their potent goitrogenic activity. The oils from rapeseed (Brassica napus) must be analyzed for potential goitrins to circumvent potential goitrogenic activity when consuming these oils []. No FDA regulations were located for permissible concentrations of glucosinolates in human food. Glucosinolates (calculated as epi-progoitrin) and goitrin are limited to not more than 4% and 0.1% (respectively) of the seed meal of Crambe abyssinica (Crambe meal) obtained after the removal of the oil and used as an animal feed ingredient (21 CFR 573.310).

 Erucic acid in rape

Rape (Brassica napus L. or Brassica campestris L.) is an annual herb of the mustard family native to Europe and is grown in the United States because it produces oil-rich seeds for cooking oil []. Rapeseed oil had been used for hundreds of years as oil for lamps and more recently as machine oil lubricant. Widespread use of rapeseed oil as a food ingredient was not considered until the late 1940s and 50s. However, early studies found that feeding high levels of rapeseed oil to rats significantly increased cholesterol levels in the adrenal glands and lipidosis in the cardiac tissue [,]. This effect was also noted in chickens, ducks and turkeys fed high levels of rapeseed oil, resulting in growth retardation, mortality, and a thickening of the epicardium and increased fibrous tissue in different areas of the myocardium []. Erucic acid was identified as the causative agent of these effects of rapeseed oil. Erucic acid is a long-chain fatty acid with one unsaturated carbon-carbon bond (C22:1). High levels of erucic acid have been liked to fatty deposit formation in heart muscle in animals []. Erucic acid is poorly oxidized by the mitochondrial β-oxidation system, especially by the myocardial cells, which results in an accumulation of erucic acid, producing myocardial lipidosis which has been reported to reduce the contractile force of the heart []. Although myocardial lipidosis due to erucic acid consumption has not been confirmed in humans, animal feeding studies confirmed the formation of myocardial lipidosis in a variety of animal species in a dose-dependent manner, which has been the standard assessment by government agencies of potential adverse effects in humans. Canola oil is obtained from Canola (Canadian oil, low acid), a rapeseed variety that was conventionally bred in the late 1970s in Canada to contain reduced levels of erucic acid and glucosinolates [,]. The FDA limits the amount of erucic acid in Canola oil to no more than 2% of the component fatty acids (21 CFR 184.1555).

Furocoumarins

Furocoumarins represent a family of natural food constituents with phototoxic and photomutagenic properties. They are found mainly in plants belonging to the Rutaceae (e.g., citrus fruits) and Umbelliferae(e.g., parsnip, parsley, celery, carrots) families. Furocoumarins are produced in response to stress, to aid plants in defense against viruses, bacteria, fungi, insects and animals, and are regarded as natural pesticides []. Concentrations may also increase after exposure to UV radiation, changes in temperature, prolonged storage, or treatment with hypochlorite or copper sulfate (Chaudhary et al., as cited in Wagstaff 1991 [], p. 270 and Beier et al., as cited in Ashwood-Smith [], p. 916).

The three most active furocoumarins in producing photodermatitis are psoralen, 5-methoxypsoralen (5-MOP, bergapten), and 8-methoxypsoralen (8-MOP, xanthotoxin or methoxsalen) []. In the presence of near UV light (320–380 nm), these three linear furocoumarins can form adducts with DNA and DNA-crosslinks. The consequences of these photoadditions to cells are cell death, mutations and chromosome aberrations []. In the presence of ultraviolet A radiation, 5-MOP and 8-MOP produce skin tumors in experimental animals. At a chronic dose of 37.5 mg/kg bw/day in the diet, 8-MOP produces increased incidences of tubular cell hyperplasia, adenomas, and adenocarcinomas of the kidney and carcinomas of the Zymbal gland in rats []. Cases of skin cancer have been reported in patients treated with 8-MOP and long-wave ultraviolet light for treatment of psoriasis or mycosis fungoides [,]. IARC has classified 5-MOP and 8-MOP plus ultraviolet radiation in group A (probably carcinogenic in humans) and in group 1 (carcinogenic to humans), respectively [,].

Citrus fruits, especially grapefruit, produce a variety of chemicals in their peels that may have adverse interactions with drugs. Typically, citrus fruit juice is produced utilizing the whole fruit, including the peel. One chemical found in the peel is bergamottin (also known as bergamot), a natural furanocoumarin that is known to inhibit some isoforms of the cytochrome P450 enzyme (CYP) 3A4 []. Inhibition of this enzyme prevents oxidative metabolism of certain drugs, resulting in an elevated concentration of a drug in the bloodstream []. Bergamot and other chemicals in citrus (e.g., lime, grapefruit, orange, lemon) oils [] are also phototoxic, causing significant toxicity to the skin when exposed to sunlight []. 5-Methoxypsoralen, the most phototoxic constituent of bergamot oil, showed mutagenic activity in bacterial assays and clastogenic effects in mammalian cells in culture when exposed to UV light [].

Celery reportedly contains 100 ppb psoralens (100 micrograms/kg) and parsnips as much as 40 ppm (40 mg/kg) []. The estimated dietary intake of furocoumarins for people eating furocoumarin-containing foods (est. 80% of the population) is 1.31 mg/day [], which is approximately 0.022 mg/kg bw/day for a 60 kg human. This is approximately 1000-fold lower than the 13-week dietary no observable adverse effect level (NOAEL) for liver toxicity in the rat (25 mg 8-MOP/kg bw/day) and 1700-fold lower than the dietary dose that has been shown to induce cancer in rats (37.5 mg/kg). Therefore, the risk of developing liver toxicity or cancer due to ingestion of psoralens in the diet is low.

In humans, the phototoxic threshold dose of furocoumarin mixtures after dietary exposure is of the order of 10 mg 8-MOP plus 10 mg 5-MOP, which is equivalent to about 15 mg 8-MOP per person. This phototoxic threshold dose is not reached by the consumption of celery roots and other conventional vegetables under normal dietary habits, which result in intake of approximately 2–8 mg furocoumarins per person []. Therefore, ordinarily dietary exposure to psoralens is not considered to be a significant risk for development of photodermatitis, albeit the margin of safety is low []. There are no FDA regulations or guidelines specific to the presence of furocoumarins in food.

4.2.7. Amylase inhibitors

Naturally occurring inhibitors of α-amylase are found in aqueous extracts of wheat, rye and kidney beans. The physiological role of α-amylase inhibitors in plants is not well understood, but may protect them against insect infestation. In mammals, some amylase inhibitors have been shown to attenuate the normal increase in blood glucose that occurs after ingestion of starch. However, since α-amylase inhibitors have been shown to be inactivated by gastric acid, pepsin or pancreatic proteinases, their potential as “starch blockers” is limited []. α-Amylase inhibitors were once added to foods as “starch blockers” to limit carbohydrate absorption for the purpose of weight loss; however, the FDA later determined that at least this use of α-amylase inhibitors was as drug, and they were consequently taken off the market [].

α-Amylase inhibitor protein is a major allergen (referred to as Asp o 2) that has been implicated in the development of occupational toxicity known as “baker’s asthma disease” []. Although α-amylase inhibitor protein is naturally found in wheat flour, it is also found in flour in which α-amylase from Aspergillus oryzae has been added to enhance carbohydrate fermentation by yeast []. Consequently, α-amylase inhibitor protein can be potentially found in baked products that are derived from sources other than wheat. Cases of food allergy have been reported in people ingesting bread containing α-amylase inhibitor protein. Symptoms of allergy include sneezing, rhinorrhea, oropharyngeal itching, hoarseness, cough and dyspnea [].

High α-amylase inhibitor activity against human salivary α-amylase has been found in wheat flour (590 units/g), whole wheat flour (351 units/g) and whole rye flour (186 units/g). Bread baking reduces the activity by 80–100%, depending on type. The activity in uncooked spaghetti (248 units/g) is reduced more than 98% by 15 minutes of boiling. Boiling of red beans for 1.5 hours reduces activity to undetectable levels []. However, α-amylase has been shown to retain some allergenic activity when heated to 200 °C (Baur et al., as cited in Phadia AB 2010 [], p. 2).

Lectins in legumes

Lectins are a group of glycoproteins that are present in high levels in legumes (e.g., black beans, soybeans, lima beans, kidney beans and lentils) and grain products [,]. Lectins can reversibly bind to carbohydrates without altering their covalent structure []. The ability of lectins to bind to and agglutinate red blood cells is well known and used for blood typing—hence the lectins are commonly called hemagglutinins. Lectins also can bind avidly to mucosal cells and interfere with nutrient absorption from the intestine []. Because the ability of the lectins to cause intestinal malabsorption is dependent on the presence of enteric bacteria, it has been hypothesized that lectins may also produce toxicity by facilitating bacterial growth in the GI tract [].

Lectins isolated from black beans can produce growth retardation when fed to rats at 0.5% of the diet, and lectin from kidney beans causes death within two weeks when fed to rats at 0.5% of the diet. Soybean lectin produces growth retardation when fed to rats at 1% of the diet. The castor bean lectin ricin (one of the most toxic natural substances known) is notorious for causing deaths of children, and has been used as an instrument of bioterrorism [].

Phytohaemagglutinin (PHA) is a lectin found in significant quantities (as much as 2.4–5% of total protein) in legumes such as red or white kidney beans, green beans and fava beans. PHA has a number of different properties, including the ability to induce mitosis, affect membrane transport and permeability to proteins, and agglutinate red blood cells. Rats fed a diet containing 6% PHA exhibit weight loss, associated with malabsorption of lipid, nitrogen and vitamin B12 []. PHA from red kidney beans inhibits sodium and chloride absorption in the rabbit ileum, indicating that PHA can affect electrolyte transport in the gut []. Symptoms of toxicity to PHA in humans such as nausea, vomiting, or diarrhea occur within three hours of ingestion. Recovery generally occurs within four or five hours of onset [].

There are no FDA regulations or guidelines restricting the presence of lectins in food, but the FDA does provide recommended cooking practices prior to consuming legumes. Concentrations of PHA (and other lectins) are higher in uncooked than cooked beans. A raw, red kidney bean can contain up to 70,000 hemagluttinating units (hau). Most lectins are reduced by moist, but not dry heat. Therefore, steaming or boiling causes a significant reduction in concentrations of lectins in beans. Boiling for at least ten minutes has been shown to reduce hau in beans by 200-fold. Because cooking temperatures under 176 °F do not destroy lectin, use of slow cooking and/or a crockpot is not advised for cooking beans [].

Anti-thiamine compounds

Substances that act on the availability of vitamins are commonly referred to as antivitamins. These include materials that can cause a deficiency of vitamins by competing with vitamins in various metabolic reactions as the result of similar chemical structure or destroying or decreasing the effects of a vitamin by modifying the molecular conformation or by forming a complex [].

Thiaminase cleaves thiamine (vitamin B1) at the methylene linkage, rendering it biologically inactive. Activity of thiaminase requires a cosubstrate—usually an amine or sulfhydryl-containing protein such as proline or cysteine. Thiaminase is found in fish, crab, clams and in some fruits and vegetables such as blueberries, black currants, red beets, Brussels sprouts and red cabbage [].

Thiamine is an essential vitamin involved in energy production. Thiamine deficiency is associated with impaired pyruvate utilization, resulting in a shortage of cellular ATP. In humans, thiamine deficiency may lead to weakness and weight loss. Severe thiamine deficiency produces “beri-beri”, a disease characterized by anorexia, cardiac enlargement, and muscular weakness leading to ataxia []. Cooking destroys thiaminases in fish and other sources. There are no FDA regulations or guidelines specific to the presence of thiaminase in food.

 Pyrrolizidine alkaloids

Pyrrolizidine alkaloids (PAs) are found in some plants of the Apocyanacae, Asteraceae, Boraginaceae, Compositae (Senecionae and Eupatoriae), Fabaceae, Leguminosae (Crotalaria), Rannuculaceae and Scrophulariaceae families. Herbs such as comfrey root and leaf (Symphytum spp.) (Figure 2), coltsfoot leaf and flower (Tussilago farfara) and borage leaf (Borago officinale), and several species of Eupatoriumtypically contain high levels of PAs. Humans are exposed to PAs through the accidental contamination of foodstuffs and intentional ingestion of PA-containing vegetables and herbal medicines. Serious incidences of illness have been reported in people consuming cereal grains that are contaminated with the seeds of PA-containing plants []. PAs are also present in milk from cows and goats and in honey [].

Root Causes of Type 1 Diabetes

Root Causes of Type 1 Diabetes

Contrary to type 2 diabetes, type 1 is not may not be rooted in insulin and leptin dysfunction caused by excessive sugar (and carbohydrate) consumption. However, over the past several years, research has given us important clues about its predisposing conditions. Two important ones that you have more or less complete control over are:

•Vitamin D deficiency. Research suggests that sun avoidance may play a major role in the development of insulin dependent diabetes. The further you move away from the equator the greater your risk of being born with, or developing type 1 diabetes. A major key to preventing type 1 diabetes in children is to ensure that pregnant mothers have optimal vitamin D stores. There is also strong evidence that this can decrease your child’s risk of autism. Once your child is born, ensuring he or she gets optimal sun exposure (and/or wise use of oral vitamin D supplementation) could virtually eliminate the risk for type 1 diabetes.

•Abnormal gut flora. An excessive focus on a germ-free environment is another potential contributing factor that impairs immune function. In 2008, animal research13 suggested that beneficial bacteria could protect against the development of type 1 diabetes. There is a good deal of evidence that a contributor to the rising rates of type 1 diabetes is raising our children in too sterile an environment. Many parents religiously use antibacterial soaps and keep their children away from the natural dirt, germs, viruses and other grime of childhood.14

Antibiotics, which kill all of the good and bad bacteria in the gut, are also overused in childhood. The lesson here is, it’s okay to let your child get dirty. Use plain soap and water for washing. Avoid antibiotics unless absolutely necessary, and feed them naturally fermented foods such as yogurt, pickles and sauerkraut.15

Root Causes of Insulin Resistance, Pre-Diabetes, Metabolic Syndrome, and Type 2 Diabetes

Type 2 diabetes involves loss of insulin and leptin sensitivity. This makes it easily preventable and nearly 100 percent reversible without drugs. One of the driving forces behind type 2 diabetes is excessive dietary fructose, which has adverse effects on all of metabolic hormones—including two key players: insulin and leptin.

There is no question in my mind that regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of insulin/leptin resistance, metabolic syndrome, and chronic diseases, including obesity, type 2 diabetes, cancer, heart disease, arthritis, and Alzheimer’s. It’s important to realize that even though fructose is relatively “low glycemic” on the front end, it actually reduces the receptor’s affinity for insulin, leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes…

Another major cause of type 2 diabetes is the consumption of the vast amount of glucose derived from the high carbohydrate diet that has been recommended for the last half century by conventional medical and media recommendations. All carbohydrates that are not fiber will be quickly metabolized into sugar, and it makes little sense to eat large amounts of sugar to keep your blood sugar lower.

The misconception of the cause of diabetes may be the biggest problem. Conventional medicine describes diabetes as a disease characterized by elevated blood sugar. This “dysregulation of blood sugar control” is typically explained as “an inability of your body to produce enough insulin.” To control diabetes with that view, it would be rational to prescribe insulin or drugs that raise insulin to counteract the elevated blood sugar. The reality however is that type 2 diabetes is NOT the result of insufficient insulin production. It’s actually the result of too much insulin being produced on a chronic basis primarily from eating the high carbohydrate, low fat diet recommended by the ADA and AHA to prevent and treat this.

This overwhelms and “deafens” your insulin receptors, hence the term “insulin resistance.” It’s the chronically elevated insulin levels that make your body “resistant” to understanding the signals sent by the insulin. This also occurs with leptin. It’s really important to realize that T2 diabetes is not caused by elevated blood sugar or “insulin deficiency” per se. The root cause is insulin and leptin resistance which is why prescribing insulin is one of the WORST things you can do for type 2 diabetes, as it will actually worsen your insulin and leptin resistance over time. You do not need more insulin. You need to restore the sensitivity of your insulin and leptin receptors by keeping their levels low!

If you’re still having trouble understanding why taking insulin is a terrible choice in type 2 diabetes consider this; when your blood sugar becomes elevated, insulin is released to direct the extra energy (sugar) into storage. A small amount is stored as a starch called glycogen, but the majority is stored as fat. Therefore, insulin’s primary role is not to lower your blood sugar, but rather to store this extra energy as fat for future needs when food may not be available. The fact that insulin lowers your blood sugar is merely a “side effect” of this energy storage process. Taking more insulin just makes you fatter!

Your body’s cells become desensitized to insulin, leptin, and other hormones, by being overexposed to these hormones—be it by eating food that causes excessive secretion, or by injection. Diabetes treatments that concentrate merely on lowering blood sugar by adding insulin therefore tend to worsen rather than remedy the actual problem of metabolic miscommunication.

As Dr. Rosedale has previously stated: “Type 2 diabetes is brought on by constantly having too much insulin and leptin circulating secondary to the same diet that has been recommended to treat diabetes and heart disease, a high carbohydrate, low-fat diet. Then giving these diabetics more insulin is adding gasoline to the fire. Doctors couldn’t be doing more harm if they tried.”

Leptin—An Oft-Ignored KEY Player in Type 2 Diabetes Development

While much conventional advice centers around insulin, leptin is another hormone that plays an integral role in the development of type 2 diabetes. Leptin is produced in your fat and other cells, and one of its primary roles is regulating your appetite and body weight. Leptin tells your brain when to eat, how much to eat, and most importantly, when to stop eating. Leptin also instructs your brain as to what to do with the available energy.

Now remember, when your blood sugar becomes elevated, insulin is released to direct the extra energy into storage—the majority of which is stored as fat, and leptin is produced in these fat cells. The more fat you have, the more leptin is produced. Furthermore, as the sugar gets metabolized in your fat cells, the fat releases further surges in leptin. This is why I typically talk about insulin and leptin resistance, as they work in tandem. Moreover, leptin is largely responsible for the accuracy of insulin signaling and whether or not you become insulin-resistant. If you’re insulin resistant, you’re more than likely leptin resistant as well, especially if you’re overweight or obese.

Why leptin resistance?

Because when you develop leptin resistance, your brain can no longer hear leptin’s signals, resulting in chronic hunger, overeating, inability to properly burn fat and, typically, obesity. Insulin resistance, and ultimately type 2 diabetes, follow suit. Just as with insulin, the only known way to reestablish proper leptin signaling is through proper diet. High consumption of carbohydrates, especially fructose, are again the prime culprit and the root cause of leptin resistance. Lack of exercise and abnormal gut flora also contribute and/or exacerbate insulin and leptin resistance. Leptin’s importance in blood glucose control and diabetes is powerfully illustrated by recent studies that show its ability, even in low doses, to lower blood glucose in both type 1 and 2 diabetics, and this is an exciting new potential treatment.

New Warning: Insulin Can Rapidly Produce Type 1 Diabetes in Type 2 Diabetics

Please understand that medications and supplements are not the answer for type 2 diabetes. Diabetes drugs fail to address the underlying problem, and many, like Avandia, can have dangerous side effects. Avandia is linked to 43 percent increased risk of heart attack and 64 percent higher risk of cardiovascular death, compared with other treatments. Instead, type 2 diabetes is best controlled by restoring your insulin and leptin sensitivities. This is done by eliminating grains and sugars—especially fructose—from your diet, getting plenty of healthy fats, exercising, and sleeping well. Further details on this will be provided below, in the treatment section.

As noted earlier, recent research published in the Journal of Clinical Endocrinology & Metabolism16 confirms what Dr. Ron Rosedale has stated for the last two decades, which is that insulin treatment can provoke otherwise reversible type 2 diabetes to progress into type 1 insulin deficient and therefore insulin-dependent diabetes. The study found that giving genetically engineered recombinant insulin to type 2 diabetics with certain genetic susceptibility can trigger their bodies to produce antibodies that destroy their insulin producing cells (pancreatic islet cells). You may not realize that all human insulin, the type typically used, is GMO or genetically modified which might be responsible for this autoimmune reaction.

Basically, it triggers an autoimmune disease response, producing a condition in which you have both type 1 and type 2 diabetes simultaneously. The average time of type 1 diabetes onset was 7.7 months. One study participant developed type 1 diabetes in just over one month! According to the authors, acute deterioration of blood glucose control after administering insulin is a warning sign of this problematic side effect. According to this study, the genes predisposing you to this autoimmune-type response to insulin are:

  • Type 1 diabetes high risk HLA class II (IDDM1), thought to play a role in about half of all type 1 diabetes cases
  • VNTR genotype (IDDM2), which is believed to predispose you to type 2 diabetes

This is yet another way conventional diabetic treatment pushes diabetics into premature death… Research17 published last year revealed that treating type 2 diabetes with insulin more than doubled patients’ risk of all-cause mortality. It also leads to:

Twice as many myocardial infarctions 1.4 time more strokes 2.1 time more neuropathy 1.4 times more cancer
1.7 time more major adverse cardiac events 3.5 times more renal complications 1.2 times more eye complications 2.2 times more deaths

Another study published in Diabetologia18, 19 in May of this year, found that diabetic cancer patients also have a significantly elevated risk of death. Diabetic patients using insulin at the time of their cancer diagnosis had a four times higher mortality rate one year after cancer diagnosis, compared to non-diabetic patients, or those who did not use insulin to control their diabetes. While this was an observational study, which means it cannot establish causality, it is worth noting nonetheless.

Dr. Rosedale has also said; “All of these increased rates of chronic diseases caused by taking insulin may be because it is doing exactly the opposite of what has been shown in many studies to reduce cancer, total mortality, and extend lifespan; reducing insulin. In fact, T2 diabetes is often considered to be a model of accelerated aging because of the high insulin. In other words, treating diabetics by overly raising insulin, either with drugs or insulin itself, is only further accelerating their aging, associated chronic diseases, and death, and should be considered malpractice.”

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Bernie – Brett Kavanaugh’s record protect corporations at the expense of workers

Bernie Sanders

Hi,

The establishment would like for you to think that the Supreme Court is an impartial judicial institution whose decisions are above politics. That was perhaps once true, but it is certainly not the case anymore.

Donald Trump just announced that he will nominate Brett Kavanaugh to the Supreme Court. Let me be absolutely clear: this nomination is a 100 percent political decision, and one that will have a profoundly negative effect on the lives of working people of this country for decades to come if Brett Kavanaugh is confirmed.

Brett Kavanaugh’s record has made it clear he will use his position on the court to protect corporations at the expense of workers, to allow corporations and the wealthy to buy elections and to undermine voting rights. Further, given the fact that Donald Trump stated repeatedly during the campaign that any nominee of his would vote to overturn Roe v. Wade, I have no doubt that is exactly what Brett Kavanaugh will do.

Simply put, nothing is more important now than doing everything in our power to stop this nomination. I intend to travel to many states around the country in opposition to this nomination. Can I count on you to work with me in this fight?

Please add your name to my petition: We must oppose Brett Kavanaugh’s nomination to the Supreme Court. This is critical to protect our democracy, so please sign now.

Here is a hard truth: for decades the far right has made it their number one goal to stack the Supreme Court with partisan ideologues. During that time, the current court has made dozens of decisions, many of them by a 5-4 vote, that have harmed women’s rights, the environment and most recently the Janusdecision, which was an attack on union rights and the standard of living of American workers.

Further, the Supreme Court has eroded voting rights, upheld Trump’s Muslim ban, and of course, by a 5-4 vote, decided Citizens United, empowering corporations and wealthy Americans to buy elections.

And it is widely suspected that a hyper-partisan Supreme Court, with Trump’s new nominee, would aim its sights directly at overturning Roe v. Wade. We can’t let this happen.

Donald Trump’s first nomination, Neil Gorsuch, has quickly become one of the most radical right-wing members of the court. The evidence suggests Brett Kavanaugh could go even further.

The damage Brett Kavanaugh could do won’t just last until the next election. He could serve on the Court for decades, making dangerous decisions for years to come.

Together we must do everything we can to win back the House, the Senate and the presidency to stop further disastrous nominees. But right now, we must do everything we can to stop the nomination of Brett Kavanaugh to the Supreme Court.

That starts with you adding your name to our petition.

Add your name to our petition to oppose the nomination of Brett Kavanaugh to the Supreme Court. Let us protect our democracy.

This will be a long fight, and I’m proud to have you with me.

In solidarity,

Bernie Sanders

ADD YOUR NAME

Health tips 7-9-2018

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Signs of the preactive/ active phase of dying and medications for terminally ill
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Eggplant and apple cider vinegar for skin cancer
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Home page / Archives
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Philippines Coconut Wine -Tuba
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Apple cider vinegar kills parasites, cleansing to the liver and prevents stroke
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DMSO, hydrogen peroxide and Vit C fight cancer cells
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Non pasteurized beers have more health benefits
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Belly fat , protein, lemon , sage tea and exercise
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Nitric Oxide Dump Exercise with nose breathing to lower blood pressure and thin blood
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Can Gout be cured permanently?
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Foods to eat and avoid when you have Gout and leg pains
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MEDICATIONS TO AVOID that worse PD (Parkinson’s disease)
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IHSS Santa Clara County pays caregivers $13 per hour to help you care for your aging parents
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Fasting, sun bathing ,Vit C, Lysine, turmeric, green tea, carrots and raw food diet to reduce tumor size
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Heartbreaking video of toddlers representing themselves in court
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Fatigue and Red (bloodshot) eyes from WebMD
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Can balsamic vinegar help with gout?
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Anti-aging and Parkinson/Alzheimer’s prevention: Enzymes and apple cider vinegar
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Mullein herb for lung and breast health – COPD signs, symptoms and diagnosis
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Eat protein-rich food when drinking alcohol to protect your stomach
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Why New Antidepressant Brintellix May Be a Killer
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Increase the body’s oxygen carrying capacity with exercise, EPO and whole foods
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Addiction, risk takers brain scan
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Philippines president Dutarte asked each town to prepare a list of drug users and pushers
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Slimy veggies, saluyot and okra fight cancer
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Misdiagnosed thyroid cancers by Dr Mercola
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Blood plasma of young mice has regenerative effect when transfused into older animals
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Restore your vision naturally y Dr. Mercola
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CAM, holistic ways on cancer, depression, heart health, women and men
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Rheumatoid Arthritis and drugs by Dr Mercola
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How Jill healed cervical cancer naturally nearly 40 years ago!
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Kidneys, lungs, immune system and virus
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Iodine prevents cancer growth; up avocado and reduce caffeine intake to prevent Thyroid cancer
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MSM powder benefits – Alzheimer is a sulfur deficiency
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Baking soda , lemon and apple cider vinegar to repair kidney damage from sugar
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Root Canal and Implants by Dr Mercola
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Infant formula, chocolate, mayonnaise, milk and cancer causing substances
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Neck pain and MTHFR gene , folate , methionine
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How important is the thymus gland in keeping your body free from diseases?
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Parasites and their effects on your immune system
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Clean up our lymps to reduce restless leg syndrome
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When will Souvenaid become available in Canada and US to treat Alzheimer’s Disease?
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Nitric Oxide for strong blood vessels’ cells , up with exercise, melons, cucumber, Vit C, E, amino acid – L-arginine, L-citrulline
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Inflammation to colitis to Alzheimer’s disease
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What are the benefits of eating chicken soup during pregnancy?
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Nominate your best doctor in the bay area
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Raising Inspired Children by Dr Joe Dispenza
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Alzheimer’s, pork and food statistics
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Lectin, gluten, stomach, fasting, toxins, wheat, and foods
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Liver cleanse to help your vision and memory
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Not patentable anti-cancer plant-fruit , soursop or Guyabano fruit, Vitamins C and B-rich
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Neurological diseases share common blood-brain barrier defects
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Cancer cells want high fat and an attack on the Pancreas
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Lung disease: COPD among white and black women
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Whole foods prevent inflammation
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Avoid chronic bronchitis with green apple, onions, garlic, vinegar and rest
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Detox your lungs from air pollution and metal toxins and for early lung cancer
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Gout, Dementia, Chelation Therapy
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Brain detox, eyes,
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Modular homes at $100k 200 sq ft vs $50k 1000 sq ft
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5 Steps to Kill Hidden Bad Bugs in Your Gut that Make You Sick by Dr Mark Hyman
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Leaky gut, leaky brain, eat your garlic and pickles by C Guthrie
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Goiter
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Curcumin: anti-parasitic, antispasmodic, anti-inflammatory, gastrointestinal effects, inhibits carcinogenesis and cancer growth
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50 Most dangerous drugs
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Characteristics of Older Male Trump Supporters
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Lung cancer in the Philippines
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Browning or caramelized sugar is a carcinogen
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Gastroparesis, Betain HCL, diabetes and stomach health
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More nitrate-reducing bacteria in saliva causes Migraine
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STDs and Virus in California
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How Jill healed cervical cancer naturally nearly 40 years ago!
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Fight VIRUS with Enzymes from pineapple and papaya, baking soda, alkaline food, calcium and magnesium from whole foods
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Own Worldgn stock, earn more and get your fitness tracker to monitor health
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Boron in Almonds and avocados for your bones
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NAC, activated charcoal , sleep and parasites
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Hiatal Hernia, Pancreatitis, Pancreatic Cancer and the Western Diet
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Dr Mercola: Tai Chi for balance and emergency prevention
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Does Consuming Low Fat Dairy Increase Parkinson’s Risk?
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How the Brain Responds to Injustice
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Philippines president Dutarte asked each town to prepare a list of drug users and pushers
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The loss of SETD8 triggers cellular senescence
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Psychological Wounds of Conflict: The Impact of War to children, young adults and soldiers
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Successful ageing
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Belly fat , protein, lemon , sage tea and exercise

Here are 6 evidence-based ways to lose belly fat.
  1. Don’t eat sugar and avoid sugar-sweetened drinks. …
  2. Eating more protein is a great long-term strategy to reduce belly fat. …
  3. Cut carbs from your diet. …
  4. Eat foods rich in fiber, especially viscous fiber. …
  5. Exercise is very effective at reducing belly fat.
More items…

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6 Simple Ways to Lose Belly Fat, Based on Science – Healthline

https://www.healthline.com/nutrition/6-proven-ways-to-lose-belly-fat

Apr 11, 2018 – Here are 6 evidence-based ways to lose belly fat. Don’t eat sugar and avoid sugar-sweetened drinks. Eating more protein is a great long-term strategy to reduce belly fat. Cut carbs from your diet. Eat foods rich in fiber, especially viscous fiber. Exercise is very effective at reducing belly fat.

Top 6 natural ways to help you lose belly fat, fast | Good Zing

http://www.goodzing.com/articles/6-natural-ways-to-lose-belly-fat-fast

Jan 9, 2018 – Discover the best natural ways to get rid of belly fat fast and develop a … are high in refined carbohydrates and sugars cause a spike in blood …

Lose Belly Fat with These Home Remedies | Reader’s Digest

https://www.rd.com/health/diet-weight-loss/home-remedies-to-lose-belly-fat/

These home remedies can flatten you lose belly fat without any fad diets or … remedies can help youreduce unwanted belly fat quickly–minus fad diets or … or replace it with a natural sweetener like stevia that won’t spike your blood sugar.

17 Incredible Home Remedies To Lose Belly Fat – Vixen Daily

http://www.vixendaily.com/diet/17-incredible-home-remedies-to-lose-belly-fat/

These Are The Best Natural Home Remedies To Lose Belly Fat. Lose belly fat with dandelion tea. Drink more cranberry juice. Try a cup of green tea. Add more hot peppers to your diet. Eat more chia seeds. Cook with coconut oil. Drink lots of ginger tea. Get proper exercise.

‘Inner fat’ is a killer lurking in your belly. Here’s how to get rid of it …

https://health.spectator.co.uk › Diet & Fitness

Jul 28, 2016 – Subcutaneous belly fat, easily spotted, is usually accompanied by ….. If you are an Oblood, then your diet should be in this order: animal fat, …

15 Home Remedies to Naturally Reduce Cholesterol

https://commonsensehome.com/naturally-reduce-cholesterol/

Apr 10, 2017 – 15 Ways to Naturally Reduce Cholesterol and Lower the Risk of Heart … the arteries either clog up and reduce or stop blood flow entirely, or get …

How to get rid of belly fat naturally: Exercise tips and remedies

https://www.medicalnewstoday.com/articles/319957.php

Nov 8, 2017 – It is, however, possible to get rid of belly fat naturally with a healthy … They also add fiber to the diet, which can help regulate blood sugar.

How to Lose Weight Naturally (22 Home Remedies) – Everyday Roots

https://everydayroots.com/weight-loss-remedies

Fat (along with protein and carbohydrates) is stored energy, plain and simple. … Blood sugar has a direct impact on your weight as it affects how hungry and … Drink about ½-1 cup every morning on an emptystomach. … Sage Tea Remedy …

How to Burn Visceral Fat | LIVESTRONG.COM

https://www.livestrong.com › Weight Management

Jul 18, 2017 – When people talk about wanting to burn belly fat, they are actually referring to … beginning of diabetes), high blood pressure, high cholesterol levels and a higher … A weight loss of five to 10 percent of your total body weight can help reduce visceral fat stores. … Natural Belly Fat RemovalWithout Exercise.

Heartbreaking video of toddlers representing themselves in court 

Infant formula, chocolate, mayonnaise, milk and cancer causing substances

Phosphatidylethanolamines in food break down to form phosphatidylethanolamine-linked Amadori products as a part of the Maillard reaction.[12] These products accelerate membrane lipid peroxidation, causing oxidative stress to cells that come in contact with them.[13] Oxidative stress is known to cause food deterioration and several diseases. Significant levels of Amadori-phosphatidylethanolamine products have been found in a wide variety of foods such as chocolate, soybean milk, infant formula, and other processed foods. The levels of Amadori-phosphatidylethanolamine products are higher in foods with high lipid and sugar concentrations that have high temperatures in processing.[12] Additional studies have found that Amadori-phosphatidylethanolamine may play a role in vascular disease,[14] act as the mechanism by which diabetes can increase the incidence of cancer,[15] and potentially play a role in other diseases as well. Amadori-phosphatidylethanolamine has a higher plasma concentration in diabetes patients than healthy people, indicating it may play a role in the development of the disease or be a product of the disease.

Using our current labeling and detection procedure, significant amounts of Amadori-PEs were detectable in infant formula, chocolate, soybean milk, processed foods (infant formula, chocolate, mayonnaise, milk, and soybean milk) contained a significant amount of Amadori-PEs. As these foods have high amounts of sugar and lipids, lipid glycation would occur during heat processing of these products. On the other hand, some foods (cream powder, yogurt, butter, margarine, tea, and coffee) did not contain any Amadori-PEs, probably because of low amounts of sugar or lipids and the relatively low temperatures used during processing of these products. Among the tested food samples, infant formulas have the most Amadori-PEs. The formulas contain PE (0.04–0.09%, w/w), and of this, 9.7–32.8 mol% was detected as the Amadori product. In contrast, human milk did not contain significant amounts of Amadori-PEs. Because the Amadori-PE generates superoxide anions and other reactive oxygen species under the presence of metal ions (11), the high glycation rate found in infant formulas may impair the nutritive value of the products.

National Institutes of Health researchers have identified a naturally occurring lipid—a waxy, fatty acid—used by a disease-causing bacterium to impair the host immune response and increase the chance of infection. Inadvertently, they also may have found a potent inflammation therapy against bacterial and viral diseases.

Lipids are known to help Francisella tularensis bacteria, the cause of tularemia, to suppress host inflammation when infecting mouse and human cells. In a new study published in the Journal of Innate Immunity, researchers from NIH’s National Institute of Allergy and Infectious Diseases found a form of the lipid phosphatidylethanoloamine, or PE, present in the bacterium. The composition of PE found in F. tularensis differs from PE found in other bacteria. In cell-culture experiments, the researchers discovered that the natural and a synthetic form of PE reduced inflammation caused by both tularemia bacteria and dengue fever virus.

Tularemia is a life-threatening disease spread to humans via contact with an infected animal or through the bite of a mosquito, tick or deer fly. Although tularemia can be successfully treated with antibiotics, it is difficult to diagnose, mainly because F. tularensisbacteria can suppress the human immune response. Dengue fever, primarily spread by Aedes aegypti mosquitoes, is rarely fatal but usually leads to a high fever, severe headache and pain throughout the body. There is no specific treatment for dengue fever.

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