catherinecherub said:I think your link is getting at the people who produce junk food within the industry.
Results from this study show that participants who were either overweight or obese and had at least two metabolic abnormalities, had the fastest decline, whilst obesity and conditions such as diabetes were individually found to have a significant effect on cognition.
http://alzheimers.org.uk/site/scripts/n ... ewsID=1305
You can be obese without eating junk food as some people are. They eat the right things but in too big a portion size. We all know that junk food as an occasional treat will not do the damage that living on these foods will create within our bodies.
Dementia sufferers come in all shapes and sizes and many have eaten healthily throughout their lives. If dementia in later life is a worry for anybody then it would seem sensible to get your diabetes, weight and other metabolic factors under control to lessen the risk.
Dementia can occur in younger people too.
http://alzheimers.org.uk/site/scripts/d ... mentID=164
Dillinger said:So, could it be the carbs that are really the problem? Just like they are for diabetes, and supposedly for heart disease and some cancers?
Dillinger[/quote
I am with you as always Dillinger. My nearly 85 year old Mum has recently been diagnosed with Alzheimers, Vascular dementia and possibly Parkinsons. Not over weight, not been told she has diabetes though I know she thinks her doctor thought she has had some high readings in the recent times. Staunchly avoids fats especially butter, full cream milk and coconut oil since 40+ years ago when a doctor told to avoid them at all costs as she had her gall bladder out. Until two months ago took no medications of any sort.
Her blood pressure was high I noticed while she chirped to the geriantologist that her doc said she had the blood pressure of a 21 year old!~
She believed that she has eaten a healthy diet, meat, three veggies mostly homegrown, no takeaways, oodles of fruit and home baked pudding and fruit cakes and no alcohol for at least 20 years.
She was frustrated with my opposing food choices but it is now too confusing for her to comprehend. Think Dad is on his way too though his decline is slower and males often fare better longer and have a slower decline into dementias I understand.
Hey ho!
Dillinger said:Here's some stuff on the benefits of low carbing and demenita
http://cauk.atkins.com/blog/colette-hei ... -diet.html
So, could it be the carbs that are really the problem? Just like they are for diabetes, and supposedly for heart disease and some cancers?
Dillinger
jopar wrote
What a load of rubbish that is...
THE KD IN ALZHEIMER DISEASE
There is growing realization that neuronal excitability is enhanced in patients with Alzheimer disease (AD; Noebels, 2011; Roberson et al., 2011). While the essential pathological processes of AD involves neuronal degeneration with accumulation of abnormal cellular products such as fibrillary plaques and tangles, recent evidence points to alterations in the function of extant neural circuits and mitochondrial homeostasis (Kapogiannis and Mattson, 2011). This view is bolstered by the higher incidence of seizures in
patients with AD as compared to the unaffected population (Palop and Mucke, 2009). Therefore, there is a rationale for hypothesizing that the KD might have a beneficial role in patients with Frontiers in Pharmacology | Neuropharmacology April 2012 | Volume 3 | Article 59 | 2Stafstrom and Rho Ketogenic diet in neurological diseases AD (Balietti et al., 2010a), in addition to the potential benefits
to the aging process as noted above. One should note, importantly, that if ketone bodies are indeed the primary mediators that counter aging and neurodegeneration in AD, implementation of the KD should be tempered by known age-related differences in
the production and extraction of ketones (i.e., this is more efficient in young animals), as well as age-specific regional differences in
ketone utilization within the brain (Nehlig, 1999). Clinical studies to date have been equivocal but promising. A randomized double-blind, placebo-controlled trial of a MCT KD resulted in significantly improved cognitive functioning in APOε4-negative patients with AD but not in patients with a APOε4 mutation (Henderson et al., 2009). In this study, the primary cognitive end-points measured were the mean change from baseline in the AD Assessment Scale-Cognitive subscale, and global scores in the AD Cooperative Study – Clinical Global Impression of Change (Henderson et al.,2009). This significant clinical improvement was considered to be secondary to improved mitochondrial function, since ketone bodies (specifically, beta-hydroxybutyrate or BHB) have been shown to protect against the toxic effects of β-amyloid on neurons in culture (Kashiwaya et al., 2000). Alternatively, the KD may actually decrease amounts of β-amyloid deposition (VanderAuwera et al., 2005). Interestingly, other diets such as the Mediterranean diet are showing some promise in AD (Gu et al.,2010), possibly through a reduction in systemic inflammation and improved metabolic profiles.
Recent studies have shown a closer linkage of AD to epilepsy. For example, animal models of AD exhibit neuronal hyperexcitability and enhanced propensity to seizures (Palop et al., 2007; Roberson et al., 2011); these models may ultimately allow for detailed analyses of both cognitive and anticonvulsant effects of the KD or other dietary manipulations such as calorie restriction.
Transgenic AD mice fed 2DG demonstrated better mitochondrial function, less oxidative stress, and reduced expression of amyloid
precursor protein and β-amyloid compared to control animals (Yao et al., 2011). Another pathophysiological mechanism hypothesized to operate in AD ties together altered mitochondrial function and glucose metabolism,i.e., accumulation of advanced glycation nd products (AGE; Srikanth et al., 2011). AGE accumulation is a process of normal aging that is accelerated in AD; proteins are non-enzymatically glycosylated and this cross-linking of proteins accentuates their dysfunction. One proposed mechanism is increased ROS and free radical formation, which, as discussed above, hampers mitochondrial function. The intriguing possibility that AGE inhibitors (e.g., aminoguanidine, tenilsetam, carnosine) could act in concert with the KD or antioxidants in retarding AD progression remains speculative at this time. Thus, there is growing evidence that the KD may be an effective treatment for AD through a variety of metabolism-induced mechanisms that reduce oxidative stress and neuroinflammation, and enhance bioenergetic profiles – largely through enhanced mitochondrial functioning. However, caution should be exercised in extrapolating findings in animals to humans, as discrepancies in terms of both clinical efficacy and untoward side-effects have been noted. For example, adverse reactions to calorie restriction have been reported in some rodent models (Maalouf et al., 2009),and in hippocampus, abnormal morphological synaptic changes have been observed in CA1 stratum moleculare (Balietti et al., 2008).
Clinical studies to date have been equivocal but promising. A randomized double-blind, placebo-controlled trial of a MCT KD resulted in significantly improved cognitive functioning in APOε4-negative patients with AD but not in patients with a APOε4 mutation (Henderson et al., 2009).
phoenix said:who did not have the APOE allele*
The research, published on-line this week in the journal Neurology, assessed about 2300 Swedish men [1]. At age 50, these men underwent a ‘glucose tolerance test’ (they were ‘dosed’ with glucose and their insulin and sugar levels were monitored subsequently). The men were assessed again at 70 and 82 years of age for a variety of things including presence of Alzheimer’s disease and what is known as ‘vascular dementia’ (dementia caused by problems with the circulation to the brain).
Analysis of the data collected in this study revealed two main things:
1. Impaired glucose tolerance was associated with a significantly increased risk of vascular dementia.
2. A ‘blunted’ insulin response (thought by the authors to be a sign of inadequate insulin secretion) was found to be associated with an increased risk of Alzheimer’s disease.
Finding number 1 is in keeping with previous work mentioned above and in my previous blog last month. However, finding 2 is not.
Just to recap, I previously suggested that HIGH levels of insulin may lead to high levels of amyloid-beta in the brain and therefore enhanced risk of Alzheimer’s disease. This more recent study, if anything, found that LOW insulin levels were associated with an increased Alzheimer’s disease risk.
Reading in the paper in search of an explanation I discovered that the authors reference previous work that has found a U-shaped association between insulin levels and Alzheimer’s disease risk [2]. In other words, both relatively high and low levels of insulin are linked with an increased risk of this condition.
Risk of Alzheimer’s disease is believed to be partly genetically determined. One risk factor appears to be the presence of something known as APOE E-4 in an individual’s genetic makeup.
The relationship between lowered insulin response and enhanced Alzheimer’s disease risk was only found in individuals without APOE E-4 (i.e. those at generally low risk). On the other hand, in individuals WITH APOE E-4 (generally high risk individuals), HIGHER insulin levels were associated with INCREASED risk.
Making sense of this is not easy, as it seems that the relationship between insulin and risk of Alzheimer’s disease is partly dictated by genetic factors and quite complex.
Nevertheless, whatever one’s genetic make-up, it seems that optimising insulin levels (not too high, not too low) makes sense for those seeking to reduce the risk of Alzheimer’s disease and dementia. One strategy here (again) is to ensure the diet is low in foods which disrupt blood sugar. This should help, for obvious reasons, to keep insulin levels from rising too high. Such a diet may also, as it happens, reduce the risk of ‘exhaustion’ of the cells in the pancreas that make insulin (known as the ‘beta’ cells). So this diet should reduce the risk of insulin levels getting too low too.
lucylocket61 said:I have noticed with elderly people that they are often malnourished.
So I go along with the thinking that adequate amounts of nourishing food are a key factor here. Starvation, at any age will affect cognition and brain function generally.
Unfortunately the elderly are often offered meals which are highly processed, pre-packaged, and low in nutrients. They are then given high-carb Build-up type drinks. Neither of these are providing a balanced nutritious diet.
So I think we need to remember that the elderly are seldom on a level playing field here. High carb, or high protein or high fat is not the same for them as for younger people not dependant on pre-cooked processed food. The definition of 'High' is from a different starting point. And their ability to process food, plus interactions with medication affecting their digestion and absorption, can be a major factor in their weight loss and malnutrition.
So the elderly, as with all of us, need a diet with sufficient carbs, fats and protein for their needs. Which may well mean higher than they are having now, but it will bring them up to the levels they should be having. Not higher as in "higher than an average person"
All these terms like "higher" are relative to what they are being compared to. I f their intake is lower than they need, then 'higher' brings them up to 'average'.
http://www.dietetics.co.uk/article-undernutrition-in-the-elderly.asp
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