Saturday, August 26, 2017

The case for a breakfast feast

The case for a breakfast feast: "Having the largest meal in the morning appears to have advantages for weight control compared with having a large meal in the evening, she said, since the digestive process and the action of insulin, the pancreatic hormone that the body uses to process the sugars in carbohydrates and store glucose, appear to be at their peak performance early in the day. As a result, “our body can use the nutrients as a source of energy the easiest,” Kahleova said.

A person eating identical meals at different times of the day might deposit more fat after an evening meal than a morning meal, she said.

That’s because insulin action is more efficient in the morning, experts say. “If you give a healthy individual a big bolus of glucose in the morning, the blood glucose might stay high one or two hours before coming back to normal,” said Dr. Satchidananda Panda, a professor at the Salk Institute for Biological Studies in San Diego. “You take that same normal healthy individual and give them the same bolus of glucose late at night, and now the pancreas is sleeping — literally — and cannot produce enough insulin, and blood glucose will stay high up to three hours.” Doctors once called this “evening diabetes,” he said."



'via Blog this'

Hunter-gatherers' seasonal gut-microbe diversity loss echoes our permanent one -- ScienceDaily

Hunter-gatherers' seasonal gut-microbe diversity loss echoes our permanent one -- ScienceDaily:



More evidence that our intestinal microbes are profoundly influenced by the foods we eat -- or don't: The gut ecosystems of members of a small group of hunter-gatherers inhabiting Tanzania's Rift Valley show a strong cyclicality consistent with the population's seasonally changing diet.
A study led by researchers at the Stanford University School of Medicine is the first to look at seasonal variations in the gut-microbial composition, or microbiota, of the Hadza, one of the world's few remaining traditional hunter-gatherer populations. The findings confirm that the Hadza microbiota is more diverse than, and substantially different from, that of industrialized countries' urban-dwelling denizens.

Thursday, August 03, 2017

New Research Discovers That Depression Is An Allergic Reaction To Inflammation

New Research Discovers That Depression Is An Allergic Reaction To Inflammation:



"New research is revealing that many cases of depression are caused by an allergic reaction to inflammation.  Tim de Chant of NOVA writes: “Inflammation is our immune system’s natural response to injuries, infections, or foreign compounds. When triggered, the body pumps various cells and proteins to the site through the blood stream, including cytokines, a class of proteins that facilitate intercellular communication.  It also happens that people suffering from depression are loaded with cytokines.”  Inflammation is caused by obesity, high sugar diets, high quantities of trans fats, unhealthy diets in general, and other causes.



 By treating the inflammatory symptoms of depression — rather than the neurological ones — researchers and doctors are opening up an exciting new dimension in the fight against what has become a global epidemic.  Caroline Williams of The Guardian writes: “The good news is that the few clinical trials done so far have found that adding anti-inflammatory medicines to antidepressants not only improves symptoms, it also increases the proportion of people who respond to treatment, although more trials will be needed to confirm this. There is also some evidence that omega 3 and curcumin, an extract of the spice turmeric, might have similar effects. Both are available over the counter and might be worth a try, although as an add-on to any prescribed treatment – there’s definitely not enough evidence to use them as a replacement.”"



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Thursday, June 29, 2017

Tau, insulin resistance, and Alzheimer's

"Much ado has been made of the neuronal damage inflicted by aggregates of tau, but what about the cost of losing normal tau protein to these proteopathic snarls? In the June 26 Journal of Experimental Medicine, researchers led by David Blum of the University of Lille in France made the case that loss of tau function triggers insulin resistance in the brain. In tau knockout mice, hippocampal neurons responded sluggishly to insulin, laying low synaptic plasticity. Metabolic disturbances extended beyond the brain: The mice overate, were obese, and tolerated glucose poorly. The researchers proposed that loss of normal tau function in early stages of Alzheimer’s could explain the brain insulin resistance observed in some people with the disease. They claim it could even contribute to systemic metabolic disorders—such as Type 2 diabetes—that emerge prior to cognitive symptoms."

http://www.alzforum.org/news/research-news/loss-tau-function-triggers-insulin-resistance-brain

Sunday, March 19, 2017

Hard choices? Ask your brain's dopamine

Hard choices? Ask your brain's dopamine: Researchers have learned how dopamine governs ongoing decisions, yielding insights into Parkinson's, drug addiction.



Say you're reaching for the fruit cup at a buffet, but at the last second you switch gears and grab a cupcake instead. Emotionally, your decision is a complex stew of guilt and mouth-watering anticipation. But physically it's a simple shift: instead of moving left, your hand went right. Such split-second changes interest neuroscientists because they play a major role in diseases that involve problems with selecting an action, like Parkinson's and drug addiction.
In the March 9, 2017 online publication of the journal Neuron, scientists at the Salk Institute report that the concentration of a brain chemical called dopamine governs decisions about actions so precisely that measuring the level right before a decision allows researchers to accurately predict the outcome. Additionally, the scientists found that changing the dopamine level is sufficient to alter upcoming choice. The work may open new avenues for treating disorders both in cases where a person cannot select a movement to initiate, like Parkinson's disease, as well as those in which someone cannot stop repetitive actions, such as obsessive-compulsive disorder (OCD) or drug addiction.
"Because we cannot do more than one thing at a time, the brain is constantly making decisions about what to do next," says Xin Jin, an assistant professor in Salk's Molecular Neurobiology Laboratory and the paper's senior author. "In most cases our brain controls these decisions at a higher level than talking directly to particular muscles, and that is what my lab mostly wants to understand better."

Saturday, February 25, 2017

Attention Deficit Disorders and Sleep/Arousal Disturbance

THOMAS E. BROWNa AND WILLIAM J. MCMULLEN, JR.b
aClinic for Attention and Related Disorders, Yale University School of Medicine,
New Haven, Connecticut 06519, USA
bCalifornia Pacific Epilepsy Center, San Francisco, California 94115, USA
ABSTRACT: Many children, adolescents, and adults with Attention Deficit Disorders
report chronic difficulties with falling asleep, awakening and/or maintaining
adequate daytime alertness. These problems may be due to a variety of
factors, including environment, lifestyle, and psychiatric comorbidities.
Impairments in sleep/arousal may also be related more directly to the underlying
pathophysiology of ADD. This chapter describes clinical manifestations
of sleep/arousal problems often associated with ADD and reviews behavioral
and medication options for treatment.
KEYWORDS: ADD; ADHD; Sleep disturbances; Sleep disorders.



"Given the above, it is not surprising that a fair degree of overlap exists between
these two disorders, though the rates of sleep disturbance in children with attention
deficit/hyperactivity disorder (ADHD) is much higher than one would expect even
given the high prevalence of sleep problems in the general school-age cohort. Ball
et al.
9 have reported that more than 50% of children with ADHD have difficulty falling
asleep. Stein10 reported that moderate to severe sleep problems occurred at least
once a week in nearly 20% of children with ADHD compared to 13.3% of psychiatric
controls, and 6.2% of pediatric controls."



[...]



Adolescent and adult patients too may suffer from inadequate wind-down routines
to prepare for sleep or from ruminative worry, or from evening family conflicts.
Some report that they remain awake primarily due to becoming distracted by activity
that is inconsistent with sleep (reading, surfing the internet, socializing). For some it
is actually easier to concentrate in the evening when background environmental
stimulation may be reduced relative to the targeted activity. Attempts at daytime
attention to target material may be thwarted by frequent interruption by distracting
background activity, while evening activity is both more stimulating than sleep (e.g.,
it is the distractor), and less often interrupted by competing stimuli. These patients
sometimes are able to fall asleep when they so engage, but establish behavior patterns
over time that preclude adequate sleep. Others may attempt to self medicate
sleep disturbance by using over the counter sleep aids or alcohol. These attempts are
often less than effective because they may not work, they may contribute to exacerbation
of attention problems, and they may alter the quality of sleep attained.25,26
Attention to proper sleep hygiene (discussed later in this chapter) and avoidance of
potentially maladaptive behavior patterns may offer some relief from problems falling
asleep in these patients.
Other patients with ADD report a lifelong pattern of consistently becoming more
alert in the evening, feeling more energized and more ready to engage in work or
social activities after dark than in the daytime. These individuals often describe a
pattern of difficulty falling asleep until very late at night; as preschoolers they may
not have been able to settle and fall into sleep until 10 or 11 P.M. most nights. As
adolescents or adults they may chronically feel restless and unable to sleep until 2 or
274 ANNALS NEW YORK ACADEMY OF SCIENCES
3 A.M. or later. Attention to proper sleep hygiene may help these patients, but they
may continue to experience delayed onset of sleep due to internal restlessness, even
in the absence of maladaptive behavioral patterns.
At present, it is not clear how these problems in getting to sleep are related to the
pathophysiology of ADD. Dahl has emphasized that there is a strong relationship
between the control of sleep and the regulation of mood and behavior in waking
states, yet he notes that “Our current knowledge of these complex relationships
between sleep, development and psychiatric well-being is at an embryonic state.”17
These issues are discussed later in this chapter



http://www.drthomasebrown.com/pdfs/ef-conflict.pdf

Sunday, February 19, 2017

The interaction between nutrition and the brain and its consequences for body weight gain and metabolism; studies in rodents and men. - PubMed - NCBI

The interaction between nutrition and the brain and its consequences for body weight gain and metabolism; studies in rodents and men. - PubMed - NCBI

The interaction between nutrition and the brain and its consequences for body weight gain and metabolism; studies in rodents and men.
la Fleur SE1, Serlie MJ2.
Author information
Abstract
Aberrant feeding behavior can lead to obesity and obesity-related medical consequences, such as insulin resistance and diabetes. Although alterations in glucose metabolism (i.e. insulin resistance), in the presence of excessive fat tissue are often explained by the consequences of dysfunctional adipose tissue, evidence is emerging that also altered brain functions might be an important determinant of insulin resistance. In this review, we provide an overview of how feeding behavior and obesity interact with brain circuitry and how these interactions affect glucose metabolism. Because brain circuitries involved in food intake have been shown to partly control glucose metabolism as well, targeting these circuitries in obese subjects might not only affect food intake and body weight but also glucose metabolism.

Wednesday, February 08, 2017

Do Dopaminergic Impairments Underlie Physical Inactivity in People with Obesity? - PubMed - NCBI

Do Dopaminergic Impairments Underlie Physical Inactivity in People with Obesity? - PubMed - NCBI: Do Dopaminergic Impairments Underlie Physical Inactivity in People with Obesity?
Kravitz AV1, O'Neal TJ2, Friend DM2.
Author information
Abstract
Obesity is associated with physical inactivity, which exacerbates the negative health consequences of obesity. Despite a wide consensus that people with obesity should exercise more, there are few effective methods for increasing physical activity in people with obesity. This lack is reflected in our limited understanding of the cellular and molecular causes of physical inactivity in obesity. We hypothesize that impairments in dopamine signaling contribute to physical inactivity in people with obesity, as in classic movement disorders such as Parkinson's disease. Here, we review two lines of evidence supporting this hypothesis: (1) chronic exposure to obesogenic diets has been linked to impairments in dopamine synthesis, release, and receptor function, particularly in the striatum, and (2) striatal dopamine is necessary for the proper control of movement. Identifying the biological determinants of physical inactivity may lead to more effective strategies for increasing physical activity in people with obesity, as well as improve our understanding of why it is difficult for people with obesity to alter their levels of physical activity.

Saturday, February 04, 2017

Exercise can help adults better cope with ADHD symptoms

Exercise can help adults better cope with ADHD symptoms: Exercise, even a small amount, can help alleviate symptoms of ADHD in adults, according to a new study. About 6 percent of American adults report symptoms consistent with attention deficit hyperactivity disorder, or ADHD, which lead to anxiety, depression, low energy and motivation, poor performance at work or school and also increased traffic accidents.



The study tested 32 young men with elevated ADHD symptoms who cycled at a moderate intensity for 20 minutes on one day, and on another day sat and rested for 20 minutes as a control condition. The participants were asked to perform a task requiring focus both before and after the different conditions, and researchers noted leg movement, mood, attention and self-reported motivation to perform the task.
As a result, researchers found that it was only after the exercise when the participants felt motivated to do the task; they also felt less confused and fatigued and instead felt more energetic. Interestingly, leg movements and performance on the task did not change after the exercise--rather, the exercise helped the young men feel better about doing the task.
These findings are consistent with prior research that shows a single bout of exercise helps people feel more energetic, said O'Connor, who is also co-director of the UGA Exercise Psychology Laboratory. The results suggest that young men who have symptoms of ADHD can benefit psychologically from the short workouts, similar to the benefits enjoyed by typical adults who work out.
"The reduced feelings of confusion and increased motivation to perform a cognitive task suggest that other types of acute exercise also may benefit cognitive performance," added study co-author Kathryn Fritz, a UGA doctoral student who completed the study as part of her master's thesis. "We speculate that a different mode or duration or intensity of exercise, other than a boring cycle ride in a sterile lab, may show larger cognitive effects for those suffering from ADHD symptoms."

Thursday, January 26, 2017

Zinc Supplements Could Help Treat ADHD

Zinc Supplements Could Help Treat ADHD:



An article published in BMC Psychiatry this week shows that zinc supplements could increase the effectiveness of stimulants used to treat children with attention deficit hyperactivity disorder (ADHD).



"The effects of ADHD on individual children differ, but symptoms include inattention, hyperactivity and impulsiveness. Stimulants are the most common treatment prescribed, but recent findings that vitamin and mineral deficiencies correlate with ADHD suggest that dietary supplements could also play a role in disease management.





Researchers from Iran carried out a controlled trial to assess the benefits of prescribing supplementary zinc alongside the more conventional methylphenidate treatment. They found that children taking additional zinc sulphate on a daily basis improved faster than those taking a placebo.
"The efficacy of zinc sulphate to increase the rate of improvement in children, seems to support the role of zinc deficiency in the pathogenesis of ADHD," say the authors."

Thursday, December 22, 2016

New research appears to point to link between vitamin D and autism

New research appears to point to link between vitamin D and autism:

New research has found that a vitamin D deficiency in pregnancy is linked to an increased risk of autism traits in children.

Tuesday, October 04, 2016

Fat vs sugar craving gene?

Scientists discover ‘fat-craving gene’ after hosting all-you-can eat chicken korma buffet. http://tiny.iavian.net/com6

Friday, September 30, 2016

Health Correlator: Niacin turbocharges the growth hormone response to anaerobic exercise: A delayed effect

Health Correlator: Niacin turbocharges the growth hormone response to anaerobic exercise: A delayed effect:



Niacin is also known as vitamin B3, or nicotinic acid. It is an essential vitamin whose deficiency leads to pellagra. In large doses of 1 to 3 g per day it has several effects on blood lipids, including an increase in HDL cholesterol and a marked decreased in fasting triglycerides. Niacin is also a powerful antioxidant.

Among niacin’s other effects, when taken in large doses�of 1 to 3 g per day, is an acute elevation in growth hormone secretion. This is a delayed effect, frequently occurring 3 to 5 hours after taking niacin. This effect is independent of exercise.

It is important to note that large doses of 1 to 3 g of niacin are completely unnatural, and cannot be achieved by eating foods rich in niacin. For example, one would have to eat a toxic amount of beef liver (e.g., 15 lbs) to get even close to 1 g of niacin. Beef liver is one of the richest natural sources of niacin.

Thursday, September 29, 2016

Lowering the Bar on the Low-Fat Diet | JAMA | JAMA Network

Lowering the Bar on the Low-Fat Diet | JAMA | JAMA Network:

David S. Ludwig, MD, PhD1

The recent revelation that the sugar industry attempted to manipulate science in the 1960s1 has once again focused attention on the quality of the scientific evidence in the field of nutrition and how best to prevent diet-related chronic disease.



 Beginning in the 1970s, the US government and major professional nutrition organizations recommended that individuals in the United States eat a low-fat/high-carbohydrate diet, launching arguably the largest public health experiment in history. Throughout the ensuing 40 years, the prevalence of obesity and diabetes increased several-fold, even as the proportion of fat in the US diet decreased by 25%. Recognizing new evidence that consumption of processed carbohydrates—white bread, white rice, chips, crackers, cookies, and sugary drinks—but not total fat has contributed importantly to these epidemics, the 2015 USDA Dietary Guidelines for Americans essentially eliminated the upper limit on dietary fat intake.2 However, a comprehensive examination of this massive public health failure has not been conducted. Consequently, significant harms persist, with the low-fat diet remaining entrenched in public consciousness and food policy. In addition, critical scientific questions have been muddled.



[...]




To facilitate this change, the Healthy People 2000 goals included a call to the food industry to increase from 2500 items “to at least 5000 brand items the availability of processed food products that are reduced in fat.” The food industry followed suit, systematically replacing fat in food products with starch and sugar.

As a result of these efforts, dietary fat decreased to near the recommended limit of 30% total energy. But contrary to prediction, total calorie intake increased substantially, the prevalence of obesity tripled, the incidence of type 2 diabetes increased many-fold, and the decades-long decrease in cardiovascular disease plateaued and may reverse, despite greater use of preventive drugs and surgical procedures. However, other changes in diet (such as meals away from home) and lifestyle (such as physical activity level) may have influenced these trends.

Recent research suggests that the focus on dietary fat reduction has directly contributed to this growing burden of chronic disease.2,69 In contrast to older, cross-sectional designs, high-quality prospective observational studies consistently show that total fat intake does not predict change in body fat, after controlling for confounding and reverse causation. Some foods previously relegated to the top of the pyramid because of high fat content (nuts, full-fat yogurt) are associated with lower rates of weight gain than common high-carbohydrate foods (processed grains, potato products, sugary beverages).9 Moreover, meta-analyses of clinical trials report that low-fat diets are inferior to comparisons controlled for treatment intensity, including low-carbohydrate diets,6 Mediterranean diets, and all higher-fat diets. Of particular importance, the major low-fat diet studies, such as the Women’s Health Initiative clinical trial and Look Ahead, failed to reduce risk for heart disease despite use of lower-intensity control conditions. In contrast, the PREDIMED study was terminated early when cardiovascular disease incidence decreased more rapidly than expected in the higher-fat diet groups compared with the low-fat control. Consistent with these findings, men and women adhering to low-fat/high-carbohydrate diets had higher, not lower, rates of premature death, although the type of dietary fats consumed importantly modified risk.7

One reason for the apparent failure of low-fat diets is that they may elicit biological adaptations—increasing hunger, slowing metabolic rate, and other hallmarks of the starvation response—that antagonize ongoing weight loss. Preliminary studies suggest that the reduced insulin secretion with low-carbohydrate and low-glycemic-index diets may attenuate these adaptations, facilitating long-term weight-loss maintenance and reducing diseases associated with hyperinsulinemia (the carbohydrate-insulin model).8