Showing posts with label geriatric nutrition. Show all posts
Showing posts with label geriatric nutrition. Show all posts

1.7.11

Dr. Barry Groves - Free The Animal

Dr. Barry Groves | Free The Animal
Despite following this shockingly high-fat diet for more than 40 years, Barry now weighs 6lb less than he did on his wedding day in 1957 when he tipped the scales at 11st 7lb.
He and Monica break every single diet diktat that has been trumpeted as “healthy eating”. And yet, here they are, trim, fit and full of beans, albeit metaphorical ones. How on earth do they do it? And where are the rest of us – eating piles of fruit and veg, and steering clear of cholesterol-laden butter – going wrong? After all, we’ve never been subject to so much education on good dietary practice, and yet prey to so many illnesses, ranging from diabetes to heart disease.
“Most people are eating in a way that is unnatural to us as a species,” says Barry, who holds a doctorate in nutritional science and has just written a book called Trick and Treat: How Healthy Eating Is Making Us Ill. “We’re a carnivorous species – our gut is identical to that of a big cat. Yet we’re encouraged to eat foods that have been padded out with modified starch and vegetable oils, and complex carbohydrates such as bread, pasta and rice, which have all been labelled healthy – but not the fatty meat that our body actually recognises.”

Barry Groves Phd - interview 'What is Needed For Low-Carb Diet Recognition'

Interview here - Moved to LivinLaVidaLowCarb.com/Blog: Groves: 'Population-Led Revolt' Needed For Low-Carb Diet Recognition


Dr. Barry Groves personally grew to appreciate the role of dietary fat
Barry Groves Pdh - website

Extract - From Jimmy Moore,  LivinLaVidaLowCarb show:

There are so many truly remarkable and fascinating people who work behind-the-scenes to share what they have personally learned and studied about livin' la vida low-carb. I've been privileged enough to interview quite a few of these people over the past couple of years and I have another incredible interview to share with you today.

Several of you e-mailed me to request I e-mail Dr. Barry Groves from Great Britain about the work he is doing on behalf of the low-carb lifestyle. The more I started reading http://www.second-opinions.co.uk, I couldn't believe I hadn't heard of him before! Well, let's just say I know who he is now and I'm honored to have had the opportunity to ask him a few questions about livin' la vida low-carb.

Should we be eating more fat? - Telegraph UK

Healthy food: Should we be eating more fat? - Telegraph

Healthy food: Should we be eating more fat?

A controversial new book claims healthy eating makes us more susceptible to disease, says Victoria Lambert

Fat content: Barry Groves with the foods he believes help him to stay healthy
Fat content: Barry Groves with the foods he believes help him to stay healthy Photo: CLARA 

MOLDEN
For breakfast, Barry Groves had an extra large egg and a 3oz slice of liver, fried in lard. He washed it down with a cup of cocoa made with double cream.
At lunch, Barry, 72, who lives near Oxford with his wife Monica, 70, will enjoy pork chops, with the fat left on, plus a few green vegetables in butter.
Finally, the couple will have a light supper consisting of cheese with a home-grown apple or pear, topped with cream, followed by more cocoa.
Despite following this shockingly high-fat diet for more than 40 years, Barry now weighs 6lb less than he did on his wedding day in 1957 when he tipped the scales at 11st 7lb.
He and Monica break every single diet diktat that has been trumpeted as “healthy eating”. And yet, here they are, trim, fit and full of beans, albeit metaphorical ones. How on earth do they do it? And where are the rest of us – eating piles of fruit and veg, and steering clear of cholesterol-laden butter – going wrong? After all, we’ve never been subject to so much education on good dietary practice, and yet prey to so many illnesses, ranging from diabetes to heart disease.
“Most people are eating in a way that is unnatural to us as a species,” says Barry, who holds a doctorate in nutritional science and has just written a book called Trick and Treat: How Healthy Eating Is Making Us Ill. “We’re a carnivorous species – our gut is identical to that of a big cat. Yet we’re encouraged to eat foods that have been padded out with modified starch and vegetable oils, and complex carbohydrates such as bread, pasta and rice, which have all been labelled healthy – but not the fatty meat that our body actually recognises.”

He says this is why we don’t know when to stop eating: “Try to eat too much fat – cheese, say – and your body will quickly tell you when it has had enough. But when you eat processed, 'low fat’ food, your body never gets the message it has had enough, so doesn’t tell the mind it is full.”

Many people are familiar with the idea of a high-fat, low-carb diet, such as that practised by the Groves – it is not dissimilar from the Atkins diet. The couple took it up initially in 1962, after piling on the pounds as newlyweds.

But Barry believes the way he eats is healthy, too. His cholesterol measures 8.2mmol (millimols per litre of blood) – current British Heart Foundation (BHF) advice is that people who are at high risk of, or who already have, heart and circulatory disease should aim for a total cholesterol level of less than 4mmol/l. He says, however, it would be far more risky to have a cholesterol level that measures less than 7mmol/l than to have it high. Research has linked low cholesterol levels to cancer and depression. His blood pressure is irrefutably impressive at 115/62 mmHg (millimetres of mercury.) The BHF’s target for the general population is to have a blood pressure below 140/85.

But hasn’t it been proved that too much saturated fat is bad for the heart?

“The whole premise that eating saturated fat would lead to heart disease is based on two old reports,” says Barry. “The first, in 1950, showed that if rabbits were fed a cholesterol-rich diet, it would fur up their arteries. Yet, rabbits are only designed to eat plant life, which has no cholesterol. The clogged arteries were caused by feeding them an unnatural diet. It could have been an allergic response.

“The second study was in 1953 when an American called Ansel Keyes, who charted six countries’ consumption of fat, compared with their rates of heart disease and found a perfect curve upwards when he started with Japan at the bottom (low consumption) and America at the top (high consumption). Of course, Keyes had access to data from 22 countries, but simply ignored that from 16 countries which didn’t suit his hypothesis.” Barry points out that this study is often used now to demonstrate how not to do research.

Even the long-term investigation into heart disease, the Framingham project started in 1948 by the American National Heart, Lung and Blood Institute, and now in its 60th year, has found no evidence of a link between diet and heart disease, according to Barry. “Professor Sylvan Lee Weinberg, a past president of the American College of Cardiology, said in 2003 that the low-fat, high-carbohydrate diet could no longer be defended.

“So, when you think how long we’ve been given these healthy eating guidelines and how in that time the rate of disease has gone up not down, you have to ask if our modern ailments have been caused by the very diet that was designed to stop them.”

What about those other tenets of a healthy life – five portions of fruit and veg, wholegrain cereals, soya milk, low-fat yogurts?
 
“Vegetables are not the problem,” says Barry, “but there’s no biological or chemical reason to eat them. Liver, for example, has all the minerals and vitamins we need. But fruit? The natural sugar it contains – fructose – is much more dangerous than simple glucose or table sugar. It has been linked to the rise in obesity.”

And he refuses to touch wheat. “It collects bacteria and dirt as it grows, and is impossible to clean. Then stored in silos, it is a haven for mice and rats, so it gets sprayed with insecticides. Put a wheat flower under the microscope and you’ll see traces of rat faeces.”

Soy milk is made with unfermented soya beans – “highly dangerous,” claims Barry. As for yogurts made with skimmed milk, they “lack conjugated linoleic acid, which prevents cancer”.

So how do we eat more healthily? “Eat purer foods, and ones that are more natural to us as a species. Cut down on bread and eat more fish, eggs, butter – any animal protein, anything that used to move around, that wasn’t stuck in the ground. Liver, kidneys, snails – even insects will do.”

• Trick and Treat: How Healthy Eating Is Making Us Ill by Barry Groves (Hammersmith Press) is available from Telegraph Bookshop for £11.99 plus £1.25p&p. To order, call 0870 428 4112, or go to telegraph.co.uk/bookshop

30.6.11

High cholesterol - comes with better memory in aged

Evolutionary Psychiatry: Nutrition and Alzheimer's Disease - Dangers of Insulin Resistance and Low Cholesterol
"…high cholesterol level is positively correlated with longevity in people over 85 years old, and in some cases has been shown to be associated with better memory function and reduced dementia… the cerebrospinal fluid of [Alzheimer's Disease] patients is substantially depleted in lipoproteins, cholesterol, triglycerides, and free fatty acids compared to matched controls."

We know that there is a strong correlation between insulin resistance and early Alzheimer's, and also there is an association between mitochondrial dysfunction (particularly in complex 1) and Alzheimer's. As I discussed in Basic Science: Energy is Everything and Brain Efficiency, when the mitochondria aren't happy, your brain isn't happy. Mitochondrial dysfunction is also implicated in Parkinson's Disease and ALS, both long-term and ultimately fatal degenerative conditions.

And now, a point I've made before (in Low Cholesterol and Suicide)- the brain is relatively small, but has 25% of the body's cholesterol. Cholesterol insulates neurons as part of the myelin sheath and provides the scaffold for the neural network, and is an important part of the membranes and all synapses. While much of the cholesterol used in the brain is made in the brain, there is clear evidence that apolipoprotein E (ApoE) is a big player in the game of shuttling cholesterol, fat, and antioxidants to the central nervous system from the body's main cholesterol factory, the liver. ApoE is made in nerve cells called astrocytes (who tend to and feed neurons), and ApoE allows the astrocytes to suck lipids, antioxidants, and cholesterol arriving in LDL and IDL particles from the bloodstream. Yes, astrocytes can transport LDL across the blood brain barrier.

The biggest genetic risk for Alzheimer's is being a carrier of a certain type of ApoE gene called ApoE4. Research has shown that ApoE4 is associated with reduced cholesterol uptake by the astrocytes. What has been confusing for the lipophobic medical establishment is that ApoE4 is associated with high LDL cholesterol… so it must be that nasty horrible LDL killing the brain! But the key bit to understand is that LDL cholesterol in longitudinal studies tends to drop before the development of Alzheimer's disease. Hmmm. We can't ignore the following tantalizing clue either:

…high cholesterol level is positively correlated with longevity in people over 85 years old, and in some cases has been shown to be associated with better memory function and reduced dementia… the cerebrospinal fluid of [Alzheimer's Disease] patients is substantially depleted in lipoproteins, cholesterol, triglycerides, and free fatty acids compared to matched controls.
All of us, but especially readers of a since-removed blog post that was part of the Venus-gate paleo disruption of a few weeks ago about the supposed dangers of densely packed saturated fat should have an understanding of how lipoproteins work. Lipoproteins (such as HDL, LDL, chylomicrons, and VLDL) basically look like this:

Image from Wikipedia

Lipoproteins carry fats and other delicacies through the blood. The blood is dangerous and filled with nasty things like oxygen and iron that can break down our gentle fats. We don't want our fats oxidized - so the lipoproteins tuck the fats into the inside to keep them safe and snuggly. Again, a MAJOR REASON for the particular structure of lipoproteins is to keep those fats safe and not exposed to the blood. Once fats are delivered to cell membranes, we still want to keep them safe - and cholesterol is like a bit of plate armor - it helps the fats stack more tightly, protecting them from oxidative damage and invading microbial pathogens.

Seneff et al continue to stack the evidence in their paper - dietary avoidance of fat (replaced by carbohydrate) and the increasingly zealous prescriptions for cholesterol-lowering medication has coincided with the rise in Alzheimer's Dementia and diabetes and obesity. These are only correlations, but one might consider that to be some evidence in favor of the plausible hypothesis that stripping the brain of cholesterol especially in an oxidative, hyperglycemic environment could lead to very sick neurons.

Study (2011) - no evidence that carbohydrates improve cognition in the aged

Carbohydrates for improving the cognitive performance of independent-living older adults with normal cognition or mild cognitive impairment

Plain Language Summary

There is no available evidence to support the use of any form of carbohydrate to improve cognitive performance in older adults with normal or mild cognitive impairment.

Carbohydrates consist of sugars, oligosaccharides, and polysaccharides. These components are found in a large range of foods in the diet and have variable effects on digestion, blood sugar levels, and impacts on health. Despite the evidence accumulated from biological and epidemiological studies and non-randomised clinical trials, there are still no randomised, controlled trials for analysing the efficacy and safety of carbohydrates in improving cognitive performance in this review. Thus, we need more studies on different types of carbohydrates, particularly those from fruit, vegetable and whole grain sources, for older adults with normal cognition and mild cognitive impairment in order to understand the role of this nutrient in the prevention or reduction of cognitive decline.

Abstract

Background

Mild cognitive impairment (MCI) is an intermediate state between normal cognition and dementia in which daily function is largely intact. This condition may present an opportunity for research into the prevention of dementia. Carbohydrate is an essential and easily accessible macronutrient which influences cognitive performance. A better understanding of carbohydrate-driven cognitive changes in normal cognition and mild cognitive impairment may suggest ways to prevent or reduce cognitive decline.

Objectives

To assess the effectiveness of carbohydrates in improving cognitive function in older adults.

Search strategy

We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group Specialized Register on 22 June 2010 using the terms: carbohydrates OR carbohydrate OR monosaccharides OR disaccharides OR oligosaccharides OR polysaccharides OR CARBS. ALOIS contains records from all major healthcare databases (The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS) as well as from many trial databases and grey literature sources.

Selection criteria

All randomised controlled trials (RCT) that have examined the efficacy of any form of carbohydrates in normal cognition and MCI.

Data collection and analysis

One review author selected and retrieved relevant articles for further assessment. The remaining authors independently assessed whether any of the retrieved trials should be included. Disagreements were resolved by discussion.

Main results

There is no suitable RCT of any form of carbohydrates involving independent-living older adults with normal cognition or mild cognitive impairment.

Authors' conclusions

There are no suitable RCTs on which to base any recommendations about the use of any form of carbohydrate for enhancing cognitive performance in older adults with normal cognition or mild cognitive impairment. More studies of many different carbohydrates are needed to tease out complex nutritional issues and further evaluate memory improvement.

27.6.11

The Secret to Long Life? HA Hyaluronic Acid

Uploaded by on May 20, 2009
Japanese researchers believe that the secret to a healthy and long life could be a substance called Hyaluronic Acid.
Find out more at www.coralsupreme.com

26.6.11

ApoE4 - why it increases Alzheimer's risk | The Human Genome

Why ApoE4 increases Alzheimer's risk | The Human Genome

Why ApoE4 increases Alzheimer's risk

10/4/07. By Oklahoma Medical Research Foundation 

People with the ApoE4 gene are at higher risk for developing Alzheimer's disease. A new study helps explain why this is so.
 
Approximately 15 per cent of the population carries a gene that causes their bodies to produce a lipoprotein – a combination of fat and protein that transports lipids (fats) in the blood –known as apolipoprotein (Apo) E4. People who inherit the E4 gene from one parent are three times more likely than average to develop Alzheimer's; those who get the gene from both parents have a tenfold risk of developing the disease.

Research led by scientists at the Oklahoma Medical Research Foundation has now uncovered a molecular mechanism that links the susceptibility gene to the process of Alzheimer's disease onset. The findings appear in the 11 April issue of 'The Journal of Neuroscience'.

Jordan Tang and colleagues discovered that ApoE4 (along with other apolipoproteins) attaches itself to a particular receptor on the surface of brain cells. That receptor, in turn, adheres to a protein known as amyloid precursor protein. The brain cells then transport the entire protein mass inside.

Once inside, cutting enzymes – called proteases – attack the amyloid precursor protein. These cuts create protein fragments that, when present in the brain for long periods of time, are believed to cause the cell death, memory loss and neurological dysfunction characteristic of Alzheimer's.

Although researchers have known for more than a decade that ApoE4 was involved in development of Alzheimer's, Tang's study is the first to connect the process of protein fragment formation to ApoE4.
Approximately 1 in 7 people carry the E4 variant of ApoE; the remainder of the population carry variations known as E2 and E3. These individuals have a markedly lower incidence of Alzheimer's than those who carry the E4 gene. The new study found that ApoE4 produced more protein fragments than did E2 or E3.

"ApoE4 apparently interacts better with the receptor than its cousins," said Tang. "This may explain why people who carry the E4 gene have a higher risk of developing Alzheimer's."

"These findings may allow us to investigate the possibility of therapeutic intervention at different points in the process," said Tang. For example, he said, such efforts might focus on developing a compound to interfere with the receptor's ability to adhere to ApoE4.

Adapted from a news release by Oklahoma Medical Research Foundation.
Image: Elderly woman with Alzheimer's, courtesy of Libby Welch

Further reading

He X, et al. Apolipoprotein receptor 2 and X11{alpha}/{beta} mediate apolipoprotein E-induced endocytosis of amyloid-{beta} precursor protein and {beta}-secretase, leading to amyloid-{beta} production. J Neurosci. 2007 Apr 11;27(15):4052-4060. Abstract

Links

Jordan Tang research page

ApoE4 - n-3 Fatty acid erythrocyte membrane content, APOE ... [Am J Clin Nutr. 2008] - PubMed result

n-3 Fatty acid erythrocyte membrane content, APOE ... [Am J Clin Nutr. 2008] - PubMed result

Am J Clin Nutr. 2008 Feb;87(2):449-54.

n-3 Fatty acid erythrocyte membrane content, APOE varepsilon4, and cognitive variation: an observational follow-up study in late adulthood.

Source

Department of Environmental and Occupational Medicine, University of Aberdeen, Aberdeen, United Kingdom. l.j.whalley@abdn.ac.uk

Abstract

BACKGROUND:

Evidence for an inverse relation between dietary intake of n-3 polyunsaturated fatty acids (PUFAs) and age-related cognitive decline is inconsistent. This inconsistency may arise because the relation is present only in the absence of the apolipoprotein E epsilon4 (APOE epsilon4) allele.

OBJECTIVE:

We aimed to determine the contribution of erythrocyte n-3 PUFA content to cognitive aging in the presence or absence of the APOE epsilon4 allele.

DESIGN:

We followed up 120 volunteers, born in 1936, at approximate ages of 64, 66, and 68 y. Their intelligence quotient at 11 y old was available. At first follow-up, we determined APOE genotype and measured the PUFA composition of erythrocyte membranes. Six cognitive tests were administered at all follow-ups. We related cognitive performance at approximately 64 y old and cognitive changes from approximately 64 to approximately 68 y old to erythrocyte n-3 PUFA composition on recruitment and to APOE epsilon4 allele status.

RESULTS:

Total n-3 PUFA and docosohexaenoic acid concentrations were associated with benefits for cognition at approximately 64 y old and from approximately 64 to approximately 68 y old. After adjustment for sex, APOE epsilon4 status, and intelligence quotient at 11 y old, the effects associated with total n-3 PUFA remained significant. Cognitive benefits were associated with higher erythrocyte n-3 PUFA content but were significant only in the absence of the APOE epsilon4 allele.

CONCLUSIONS:

These data are evidence of a gene x environment interaction for cognitive aging. They are relevant to the analysis of trials of n-3 PUFA supplements in cognitive aging and dementia prevention, and they support heterogeneity in cognitive aging and, possibly, in Alzheimer disease.

PMID:
18258638
[PubMed - indexed for MEDLINE]
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25.6.11

Study (2004) - more saturated fats, less carb reduces atherosclerosis in postmenopausal women

Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women

Conclusions: In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.




Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women1,2,3

Dariush Mozaffarian, Eric B Rimm and David M Herrington
1 From the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, and the Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston (DM and EBR); the Health Services Research and Development Program, Veterans Affairs Puget Sound Health Care System, Seattle (DM); the Cardiovascular Nutrition Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston (AHL and ATE); and the Section on Cardiology, Department of Internal Medicine, and the Department of Public Health Sciences, Wake Forest University, Winston-Salem, NC (DMH)