HbA1c sugar damaged blood protein – are we measuring the
most important thing.?
We urgently need
to routinely test for Fructose damage in a blood test!
A Fructose Damage Blood Test?
Reply
Tag Archives: fructose
Autoimmunity and T2D
My anecdotal experience and studies have shown me thIs:-
In cooking at oven temps this is a desirable and flavoursome reaction at some speed.
Link
A sample preview of slides for my presentation is linked here.
Publications on which the talk is based are free to download here.
Link
The Academy of Medical Royal Colleges Obesity Initiative was launched at a parliamentary reception. At this reception I was able to confirm with several members of the Steering Group that the submissions of evidence (Appendix B in their report) clearly identified Dietary Sugar as a major contributor to this epidemic of Obesity which has steadily increased since around 1980.
This was the time when we were ill-advised to eat less fat and eat more sugar generating carbohydrate foods (McGovern & COMA). Ironically it was also the time when the food industry gave us low fat options by replacing healthy fats with cheap unhealthy sugars. A 35 year obesity epidemic has ensued.
There were many notable contributors and I commend the following evidence submission (click on names for links)
Link
Key points in our paper are:-
The amyloid-β present in Alzheimer’s plaque may not be causal,
since drug-induced suppression of its synthesis led to further
cognitive decline in the controlled studies performed so far.
• Researchers have identified mitochondrial dysfunction and brain
insulin resistance as early indicators of Alzheimer’s disease.
• ApoE-4 is a risk factor for Alzheimer’s disease, and ApoE is involved
in the transport of cholesterol and fats, which are essential for signal
transduction and protection from oxidative damage.
• The cerebrospinal fluid of Alzheimer’s brains is deficient in fats and
cholesterol.
• Advanced glycation end-products (AGEs) are present in significant
amounts in Alzheimer’s brains.
• Fructose, an increasingly pervasive sweetening agent, is ten times as
reactive as glucose in inducing AGEs.
• Astrocytes play an important role in providing fat and cholesterol to
neurons.
• Glycation damage interferes with the LDL-mediated delivery of fats
and cholesterol to astrocytes, and therefore, indirectly, to neurons.
• ApoE induces synthesis of Aβ when lipid supply is deficient.
• Aβ redirects neuron metabolism towards other substrates besides
glucose, by interferingwith glucose and oxygen supply and increasing
bioavailability of lactate and ketone bodies.
• Synthesis of the neurotransmitter, glutamate, is increased when
cholesterol is deficient, and glutamate is a potent oxidizing agent.
• Over time, neurons become severely damaged due to chronic exposure
to glucose and oxidizing agents, and are programmed for apoptosis
due to highly impaired function.
• Once sufficiently many neurons are destroyed, cognitive decline is
manifested.
• Simple dietary modification, towards fewer highly-processed
carbohydrates and relatively more fats and cholesterol, is likely a
protective measure against Alzheimer’s disease.
Link
The brain is only 2% of your body mass but it contains 25% of your cholesterol. The cholesterol is vital to memory formation (synapses) and nerve protection (myelin). Our livers make 2.5g of fresh cholesterol every day to replace the losses. The liver delivers the brains fresh daily supply of cholesterol to the brain in small lipid droplets known as LDL. The empties return to the liver known as HDL with various waste products for recycling and disposal.
To get these vital supplies into the brain the LDL droplets have to cross the blood-brain barrier. The particles carry a protein label which is recognised by the receptors. The brains receptors lock onto the LDL and allow the particles to pass though into the brains astrocyte cells. These astrocytes use the cholesterol and fats in the care and feeding of the neurons and all is well with our thoughts and memories.
If we consume a lot of sugary products, especially fructose, the receptors become damaged by sugary attachments and fail to work. The LDL then builds up in the blood and the brain is starved of fat and cholesterol. All is now not well with our thoughts and memories.
This is a simplification of our biochemical papers on this matter. Other organs like the heart are also affected this way. How is it possible for an educated professionals to go on misleading us by referring to LDL as “Bad Cholesterol”?
Fructose is getting away with murder and the blame is being laid upon the good guys – fat and cholesterol.
Please click on and read our free peer reviewed medical journal publications and ask your medical advisors some tough questions about this low cholesterol ‘madness’.
“Cholesterol Lowering Therapies and Membrane Cholesterol”
Wainwright G Mascitelli L & Goldstein M R
Archives of Medical Science Vol. 5 Issue 3 p289-295 2009
“Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?”
Seneff S, Wainwright G, and Mascitelli L
Archives of Medical Science Vol. 7 Issue 1 p8-20 2011 doi: 10.5114/aoms.2011.20598
“Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet”
Seneff S., Wainwright G., and Mascitelli L.
European Journal of Internal Medicine 2011 doi:10.1016/j.ejim.2010.12.0172011
Link
Fructose Has Different Effect Than Glucose On Brain Regions That Regulate Appetite
Jan. 1, 2013 — In a study examining possible factors regarding the associations between fructose consumption and weight gain, brain magnetic resonance imaging of study participants indicated that ingestion of glucose but not fructose reduced cerebral blood flow and activity in brain regions that regulate appetite, and ingestion of glucose but not fructose produced increased ratings of satiety and fullness, according to a preliminary study published in the January 2 issue of JAMA.
JAMA and Archives Journals (2013, January 1). Fructose has different effect than glucose on brain regions that regulate appetite.
Fructose Has Different Effect Than Glucose On Brain Regions That Regulate Appetite
Link
Effects of Fructose vs Glucose on Regional Cerebral Blood Flow in Brain Regions Involved With Appetite and Reward Pathways
JAMA. 2013;309(1):63-70. doi:10.1001/jama.2012.116975Importance Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety.
Objective To study neurophysiological factors that might underlie associations between fructose consumption and weight gain.
Design, Setting, and Participants Twenty healthy adult volunteers underwent 2 magnetic resonance imaging sessions at Yale University in conjunction with fructose or glucose drink ingestion in a blinded, random-order, crossover design.
Main Outcome Measures Relative changes in hypothalamic regional cerebral blood flow (CBF) after glucose or fructose ingestion. Secondary outcomes included whole-brain analyses to explore regional CBF changes, functional connectivity analysis to investigate correlations between the hypothalamus and other brain region responses, and hormone responses to fructose and glucose ingestion.
Results There was a significantly greater reduction in hypothalamic CBF after glucose vs fructose ingestion (−5.45 vs 2.84 mL/g per minute, respectively; mean difference, 8.3 mL/g per minute [95% CI of mean difference, 1.87-14.70]; P = .01). Glucose ingestion (compared with baseline) increased functional connectivity between the hypothalamus and the thalamus and striatum. Fructose increased connectivity between the hypothalamus and thalamus but not the striatum. Regional CBF within the hypothalamus, thalamus, insula, anterior cingulate, and striatum (appetite and reward regions) was reduced after glucose ingestion compared with baseline (P < .05 significance threshold, family-wise error [FWE] whole-brain corrected). In contrast, fructose reduced regional CBF in the thalamus, hippocampus, posterior cingulate cortex, fusiform, and visual cortex (P < .05 significance threshold, FWE whole-brain corrected). In whole-brain voxel-level analyses, there were no significant differences between direct comparisons of fructose vs glucose sessions following correction for multiple comparisons. Fructose vs glucose ingestion resulted in lower peak levels of serum glucose (mean difference, 41.0 mg/dL [95% CI, 27.7-54.5]; P < .001), insulin (mean difference, 49.6 μU/mL [95% CI, 38.2-61.1]; P < .001), and glucagon-like polypeptide 1 (mean difference, 2.1 pmol/L [95% CI, 0.9-3.2]; P = .01).
Conclusion and Relevance In a series of exploratory analyses, consumption of fructose compared with glucose resulted in a distinct pattern of regional CBF and a smaller increase in systemic glucose, insulin, and glucagon-like polypeptide 1 levels.
Link
Fat Chance: Beating the odds against sugar, processed food, obesity, and disease by Robert H. Lustig
Liz & Glyn Wainwright 