Coffee and Chocolate Make You Smarter

From Inc.com

There's no longer any controversy: Every healthy diet should include at least some caffeine.

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Neuroscience continues to uncover new ways that coffee and (to a lesser extent) tea and chocolate, tend to make brains healthier and more resilient. 2019 has already seen some amazing research breakthroughs that are definitely worth sharing.

First, a joint study from the National Institute on Aging and Johns Hopkins University, and published last January in Neurochemical Research magazine, discovered that a methylxanthines--a class of chemical found in coffee, tea and dark chocolate (cacao)

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"has clear effects on neuronal network activity, promotes sustained cognitive performance and can protect neurons against dysfunction and death in animal models of stroke, Alzheimer's disease and Parkinson's disease."

That same study also discovered that xanthine metabolites--a chemical released when your brain processes caffeine, "may also contribute to the beneficial effects of coffee, tea and cacao on brain health."

Second, a meta-analysis of 11 studies on the impact of coffee on brain health and published in World Journal of Surgical Oncology showed that both coffee and tea (and thus, by extension, cacao) doesn't just reduce the risk of alzheimer's disease but also reduces the risk of brain cancer.

Finally, a groundbreaking study at Okayama University

"indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus."

Translation: caffeine makes your brain more flexible and resilient.

The big takeaway: if you want to keep your brain healthy both today and in the future as you age, you should be consuming coffee, tea, or cacao.

How much?

Well, chances are you're not consuming enough. Studies have shown that the ideal daily dosage of coffee is about six to eight 8oz cups, ideally consumed prior to 2pm so that it doesn't disturb your sleep.

If that sounds like too much coffee, consider replacing a cup or two with an ounce of dark chocolate. It need hardly be said that, for other health reasons, you should be consuming coffee, tea and cacao without sugar or creamer.  But you still get the brain-boost, regardless.

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Junk food can lead to blindness

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September 3, 2019   

Source: University of Bristol

Summary:              

An extreme case of 'fussy' or 'picky' eating caused a young patient's blindness, according to a new case report. The researchers who examined the case recommend clinicians consider nutritional optic neuropathy in any patients with unexplained vision symptoms and poor diet, regardless of BMI, to avoid permanent vision loss.         

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French fries (stock image).

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An extreme case of "fussy" or "picky" eating caused a young patient's blindness, according to a new case report published today in Annals of Internal Medicine.

                                                               

The University of Bristol researchers who examined the case recommend clinicians consider nutritional optic neuropathy in any patients with unexplained vision symptoms and poor diet, regardless of BMI, to avoid permanent vision loss.

Nutritional optic neuropathy is a dysfunction of the optic nerve which is important for vision. The condition is reversible, if caught early. But, left untreated, it can lead to permanent structural damage to the optic nerve and blindness.

In developed countries like the UK, the most common causes of nutritional optic neuropathy are bowel problems or drugs that interfere with the absorption of various important nutrients from the stomach. Purely dietary causes are less common because food supply is good, but elsewhere in the world, poverty, war and drought are linked to malnutrition and higher rates of nutritional optic neuropathy.

Clinician scientists from Bristol Medical School and the Bristol Eye Hospital examined the case of a teenage patient who first visited his GP complaining of tiredness. The link between his nutritional status and vision was not picked up until much later, and by then, his visual impairment had become permanent.

Aside from being a "fussy eater," the patient had a normal BMI and height and no visible signs of malnutrition and took no medications. Initial tests showed macrocytic anemia and low vitamin B12 levels, which were treated with vitamin B12 injections and dietary advice. When the patient visited the GP a year later, hearing loss and vision symptoms had developed, but no cause was found. By age 17, the patient's vision had progressively worsened, to the point of blindness. Further investigation found the patient had vitamin B12 deficiency, low copper and selenium levels, a high zinc level, and markedly reduced vitamin D level and bone mineral density. Since starting secondary school, the patient had consumed a limited diet of chips, crisps, white bread, and some processed pork. By the time the patient's condition was diagnosed, the patient had permanently impaired vision.

The researchers concluded that the patient's 'junk food' diet and limited intake of nutritional vitamins and minerals resulted in the onset of nutritional optic neuropathy. They suggest the condition could become more prevalent in future, given the widespread consumption of 'junk food' at the expense of more nutritious options, and the rising popularity of veganism if the vegan diet is not supplemented appropriately to prevent vitamin B12 deficiency.

Dr Denize Atan, the study's lead author and Consultant Senior Lecturer in Ophthalmology at Bristol Medical School and Clinical Lead for Neuro-ophthalmology at Bristol Eye Hospital, said: "Our vision has such an impact on quality of life, education, employment, social interactions, and mental health. This case highlights the impact of diet on visual and physical health, and the fact that calorie intake and BMI are not reliable indicators of nutritional status."

The team recommends dietary history should be part of any routine clinical examination like asking about smoking and alcohol intake. This may avoid a diagnosis of nutritional optic neuropathy being missed or delayed as some associated visual loss can fully recover if the nutritional deficiencies are treated early enough.

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Healing the Brain: Gut-brain connection helps explain obesity

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August 12, 2019

Source:

Baylor College of Medicine

Summary:

A research team reveals a previously unknown gut-brain connection that helps explain how those extra servings lead to weight gain.

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Overeating, junk food concept (stock image).

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Eating extra servings typically shows up on the scale later, but how this happens has not been clear. A new study published today in the Journal of Clinical Investigation by a multi-institutional team led by researchers at Baylor College of Medicine reveals a previously unknown gut-brain connection that helps explain how those extra servings lead to weight gain.

Mice consuming a high-fat diet show increased levels of gastric inhibitory polypeptide (GIP), a hormone produced in the gut that is involved in managing the body's energy balance. The study reports that the excess GIP travels through the blood to the brain where it inhibits the action of leptin, the satiety hormone; consequently, the animals continue eating and gain weight. Blocking the interaction of GIP with the brain restores leptin's ability to inhibit appetite and results in weight loss in mice.

"We have uncovered a new piece of the complex puzzle of how the body manages energy balance and affects weight," said corresponding author Dr. Makoto Fukuda, assistant professor of pediatrics at Baylor and the USDA/ARS Children's Nutrition Research Center at Baylor and Texas Children's Hospital.

Researchers know that leptin, a hormone produced by fat cells, is important in the control of body weight both in humans and mice. Leptin works by triggering in the brain the sensation of feeling full when we have eaten enough, and we stop eating. However, in obesity resulting from consuming a high-fat diet or overeating, the body stops responding to leptin signals -- it does not feel full, and eating continues, leading to weight gain.

"We didn't know how a high-fat diet or overeating leads to leptin resistance," Fukuda said. "My colleagues and I started looking for what causes leptin resistance in the brain when we eat fatty foods. Using cultured brain slices in petri dishes we screened blood circulating factors for their ability to stop leptin actions. After several years of efforts, we discovered a connection between the gut hormone GIP and leptin."

GIP is one of the incretin hormones produced in the gut in response to eating and known for their ability to influence the body's energy management. To determine whether GIP was involved in leptin resistance, Fukuda and his colleagues first confirmed that the GIP receptor, the molecule on cells that binds to GIP and mediates its effects, is expressed in the brain.

Then the researchers evaluated the effect blocking the GIP receptor would have on obesity by infusing directly into the brain a monoclonal antibody developed by Dr. Peter Ravn at AstraZeneca that effectively prevents the GIP-GIP receptor interaction. This significantly reduced the body weight of high-fat-diet-fed obese mice.

"The animals ate less and also reduced their fat mass and blood glucose levels," Fukuda said. "In contrast, normal chow-fed lean mice treated with the monoclonal antibody that blocks GIP-GIP receptor interaction neither reduced their food intake nor lost body weight or fat mass, indicating that the effects are specific to diet-induced obesity."

Further experiments showed that if the animals were genetically engineered to be leptin deficient, then the treatment with the specific monoclonal antibody did not reduce appetite and weight in obese mice, indicating that GIP in the brain acts through leptin signaling. In addition, the researchers identified intracellular mechanisms involved in GIP-mediated modulation of leptin activity.

"In summary, when eating a balanced diet, GIP levels do not increase and leptin works as expected, triggering in the brain the feeling of being full when the animal has eaten enough and the mice stop eating," Fukuda said. "But, when the animals eat a high-fat diet and become obese, the levels of blood GIP increase. GIP flows into the hypothalamus where it inhibits leptin's action. Consequently, the animals do not feel full, overeat and gain weight. Blocking the interaction of GIP with the hypothalamus of obese mice restores leptin's ability to inhibit appetite and reduces body weight."

These data indicate that GIP and its receptor in the hypothalamus, a brain area that regulates appetite, are necessary and sufficient to elicit leptin resistance. This is a previously unrecognized role of GIP on obesity that plays directly into the brain.

Although more research is needed, the researchers speculate that these findings might one day be translated into weight loss strategies that restore the brain's ability to respond to leptin by inhibiting the anti-leptin effect of GIP.

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Socially active 60-year-olds face lower dementia risk

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Date:

August 2, 2019

Source:

University College London

Summary:

Being more socially active in your 50s and 60s predicts a lower risk of developing dementia later on, finds a new UCL-led study published in PLOS Medicine.

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Being more socially active in your 50s and 60s predicts a lower risk of developing dementia later on, finds a new UCL-led study.

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The longitudinal study, published in PLOS Medicine, reports the most robust evidence to date that social contact earlier in life could play an important role in staving off dementia.

"Dementia is a major global health challenge, with one million people expected to have dementia in the UK by 2021, but we also know that one in three cases are potentially preventable," said the study's lead author, Dr Andrew Sommerlad (UCL Psychiatry).

"Here we've found that social contact, in middle age and late life, appears to lower the risk of dementia. This finding could feed into strategies to reduce everyone's risk of developing dementia, adding yet another reason to promote connected communities and find ways to reduce isolation and loneliness."

The research team used data from the Whitehall II study, tracking 10,228 participants who had been asked on six occasions between 1985 and 2013 about their frequency of social contact with friends and relatives. The same participants also completed cognitive testing from 1997 onwards, and researchers referred to the study subjects' electronic health records up until 2017 to see if they were ever diagnosed with dementia.

For the analysis, the research team focused on the relationships between social contact at age 50, 60 and 70, and subsequent incidence of dementia, and whether social contact was linked to cognitive decline, after accounting for other factors such as education, employment, marital status and socioeconomic status.

The researchers found that increased social contact at age 60 is associated with a significantly lower risk of developing dementia later in life. The analysis showed that someone who saw friends almost daily at age 60 was 12% less likely to develop dementia than someone who only saw one or two friends every few months.

They found similarly strong associations between social contact at ages 50 and 70 and subsequent dementia; while those associations did not reach statistical significance, the researchers say that social contact at any age may well have a similar impact on reducing dementia risk.

Social contact in mid to late life was similarly correlated with general cognitive measures.

Short exercise boosts memory

Researchers discover a gene in mice that's activated by brief periods of exercise

Date: July 2, 2019

Source:

Oregon Health & Science University

Summary:

Neuroscientists, working with mice, have discovered that a short burst of exercise directly boosts the function of a gene that increases connections between neurons in the hippocampus, the region of the brain associated with learning and memory.

  

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Neuroscientists at OHSU in Portland, Oregon, working with mice, have discovered that a short burst of exercise directly boosts the function of a gene that increases connections between neurons in the hippocampus, the region of the brain associated with learning and memory.

The research is published online in the journal eLife.

"Exercise is cheap, and you don't necessarily need a fancy gym membership or have to run 10 miles a day," said co-senior author Gary Westbrook, M.D., senior scientist at the OHSU Vollum Institute and Dixon Professor of Neurology in the OHSU School of Medicine.

Previous research in animals and in people shows that regular exercise promotes general brain health. However, it's hard to untangle the overall benefits of exercise to the heart, liver and muscles from the specific effect on the brain. For example, a healthy heart oxygenates the whole body, including the brain.

"Previous studies of exercise almost all focus on sustained exercise," Westbrook said. "As neuroscientists, it's not that we don't care about the benefits on the heart and muscles but we wanted to know the brain-specific benefit of exercise."

So the scientists designed a study in mice that specifically measured the brain's response to single bouts of exercise in otherwise sedentary mice that were placed for short periods on running wheels. The mice ran a few kilometers in two hours.

The study found that short-term bursts of exercise -- the human equivalent of a weekly game of pickup basketball, or 4,000 steps -- promoted an increase in synapses in the hippocampus. Scientists made the key discovery by analyzing genes that were increased in single neurons activated during exercise.