Optimal sodium is 3-5g/day and potassium above 2g/day

.
- in order to minimize the risk of cardio-vascular disease. This is based on thew recent study:
"Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study", by Martin O’Donnell et al., BMJ 2019; 364

These guidelines are significantly higher than the existing WHO recommendations.

Fig 3

Heat map of risk for composite of cardiovascular events or death showing lowest risk in region of moderate sodium intake 3-5 g/day and higher potassium intake and highest risk in region of extremes of sodium excretion and low potassium excretion. The reference hazard for these hazard ratios was set at a value of sodium daily excretion/intake of 5.00 g and potassium daily excretion/intake of 2.25 g (median excretion of sodium and potassium), marked as X. The overlaid lines represent joint distribution quartiles; each region contains a quarter of the analysed participants. r=0.34

Non-compliant diabetics had lower CVD risk

.


"Adherence to lipid-lowering medications and cardiovascular disease prevention in type 2 diabetes mellitus", by Karlsson, Sofia Axia, PhD thesis, University of Gothenburg, 7-Nov-2018


Quote:

Adjusted for potential confounders, risk of CV events was higher among patients with less than complete adherence to lipid lowering medications and that risk gradually increased as patient adherence declined, independent of prevention group.

Ketogenic diet protects against chemotherapy

.

"β-Hydroxybutyrate, a ketone body, reduces the cytotoxic effect of cisplatin via activation of HDAC5 in human renal cortical epithelial cells", Daisuke Mikami et al., Life Sciences
Volume 222, 1 April 2019, Pages 125-132

Quote:

Main methods

In this study, we used human renal cortical epithelial (HRCE) cells. The anti-apoptotic effect of βOHB was evaluated using flow cytometry analysis. The expression of apoptosis-related proteins and HDACs was evaluated by western immunoblot.

Key findings

The results showed that βOHB significantly reduced cisplatin-induced apoptosis in HRCE cells. Furthermore, βOHB significantly reduced cisplatin-induced cleavage of caspase-3, acetylation of histone H3, and phosphorylation of AMP-activated kinase. This anti-apoptotic effect of βOHB was markedly attenuated by an inhibitor of HDAC4/5, and βOHB-mediated suppression of cleavage of caspase3 was significantly blocked by siRNA-induced gene silencing of HDAC5.

Significance

βOHB attenuates cisplatin-induced apoptosis by activation of HDAC5 in HRCE cells, suggesting that βOHB may be a new therapeutic agent for cisplatin nephropathy.

many top scientists believe global warming theory is fraud

.



1000 Scientists Declare Man Made Global Warming Climate Change a Complete Fraud / Hoax

German Professor: NASA Has Fiddled Climate Data On ‘Unbelievable’ Scale


Quote:

Professor Dr. Friedrich Karl Ewert is a retired geologist and data computation expert. He has painstakingly examined and tabulated all NASA GISS’s temperature data series, taken from 1153 stations and going back to 1881. His conclusion: that if you look at the raw data, as opposed to NASA’s revisions, you’ll find that since 1940 the planet has been cooling, not warming.

New cancer treatment with rosiglitazone+trametinib

.

Cancer Cells Transformed into Harmless Fat in Mouse Study, By Rachael Rettner, January 15, 2019

Quote:

Then, the researchers treated the mice with two drugs: rosiglitazone, which is used in people to treat type 2 diabetes, and trametinib, an anti-cancer drug that inhibits the growth and spread of cancer cells. (Rosiglitazone belongs to a class of drugs known as thiazolidinediones, which bind to receptors that are found mainly in fat tissue and that play a role in a number of biological processes, including the formation of mature fat cells, according to a 2005 paper on the topic. People with diabetes are given the drug because the receptors that it binds to also help increase sensitivity to the hormone insulin, which is involved in regulating blood sugar levels.) The researchers in the new study found that when mice received this drug combination, the cancer cells that had broken free from the initial tumor (called "invasive cancer" cells) changed into fat cells. The drugs also suppressed the growth of the tumor and prevented further metastasis.

Climatism is a big business!

.

A must read!

"Let’s do follow the climate money!", by Paul Driessen, December 30, 2018


Quotes:

* Federal funding for climate change research, technology, international assistance, and adaptation has increased from $2.4 billion in 1993 to $11.6 billion in 2014, with an additional $26.1 billion for climate change programs and activities provided by the 2009 American Recovery and Reinvestment Act.

* The Feds spent an estimated $150 billion on climate change and green energy subsidies during President Obama’s first term.

* That didn’t include the 30% tax credits/subsidies for wind and solar power: $8 billion to $10 billion a year – plus billions more from state programs that require utilities to buy expensive “green” energy.

* Worldwide, according to the “progressive” Climate Policy Initiative, climate change “investment” in 2013 totaled $359 billion – but this “falls far short” of the $5 trillion per year that’s actually needed.

The UN’s Intergovernmental Panel on Climate Change echoes those greedy demands. It says the world must spend $2.4 trillion per year for the next 17 years to subsidize the transition to renewable energy.

Bear in mind that $1.5 trillion per year was already being spent in 2014 on Climate Crisis, Inc. research, consulting, carbon trading and renewable projects, according to the Climate Change Business Journal. With 6-8% annual growth, we’re easily looking at a $2-trillion-per-year climate industry by now.

Mechanism behind omega-6 seed oil triggering autoimmune diseases

.

Summary. The study proved the following mechanism on mice may be triggering diseases such as muscular dystrophy, rheumatoid arthritis, atherosclerosis and lupus:

1. Dietary omega-6 seed oils produces NHE,

2. NHE binds to aminoacids from the DNA, then

3. immune system reacts against that and produces antibodies against NHA and against the DNA

4. immune system attacks and destroys body's own DNA and the cells die!

First read this, to understand what NHE is:
4-Hydroxynonenal (NHE)

Specifically:

Quote:

4-Hydroxynonenal is generated in the oxidation of lipids containing polyunsaturated omega-6 acyl groups, such as arachidonic or linoleic groups,
...
Special attention must also be paid to cooking oils used repeatedly in caterings and households, because in those processes very high amounts of OαβUAs are generated and they can be easily absorbed through the diet.

And then read this:

"Protein-bound 4-Hydroxy-2-nonenal
AN ENDOGENOUS TRIGGERING ANTIGEN OF ANTI-DNA RESPONSE", by Kazuyo Toyoda et al.,
THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 282, NO. 35, pp. 25769 –25778, August 31, 2007

Quote:

Abstract

Several lines of evidence indicate that the nonenzymatic oxidative modification of proteins and the subsequent accumulation of the modified proteins have been found in cells during aging and oxidative stress and in various pathological states, including premature diseases, muscular dystrophy, rheumatoid arthritis, and atherosclerosis. Our previous work suggested the existence of molecular mimicry between antibodies raised against hydroxy-2-nonenal (HNE)-modified protein and anti-DNA autoantibodies, a serologic hallmark of systemic lupus erythematosus (SLE). In the present study, we investigated the possible involvement of HNE-modified proteins as the endogenous source of the anti-DNA antibodies.

...

4-Hydroxy-2-nonenal (HNE), one of the most prominent lipid peroxidation-specific aldehydes, is believed to be largely responsible for the cytopathological effects observed during oxidative stress (4, 5). HNE exerts these effects because of its facile reactivity with biological materials, including proteins (Fig. 1) (5). Upon reaction of the protein, HNE specifically reacts with nucleophilic amino acids, such as cysteine, histidine, and lysine, to form stable Michael addition adducts possessing the cyclic hemiacetal structure (5). Previously, we raised the anti-HNE monoclonal antibodies (mAbs), which enantios-electively recognized the (R)-HNE-histidine Michael adducts (11), and unexpectedly found that the sequence of an anti-HNE mAb was highly homologous to the anti-DNA autoantibodies (12). In addition, we characterized the ability of the mAb to recognize DNA and identified the 4-Oxo-2-nonenal (ONE)-modified 2′-deoxynucleoside (7-(2-oxo-heptyl)-substituted 1,N2-etheno-type 4-oxo-2-nonenal-2′-deoxynucleoside) as an alternative epitope. Based on these findings, we proposed the hypothesis that post-translational protein modification with lipid peroxidation products, such as HNE, could serve as an immunological trigger for the production of anti-DNA autoantibodies in autoimmune diseases.

[thanks @TuckerGoodrich]

We don't need no plants antioxidants!

.
- probably! As hinted in the following study:

Dietary (Poly)phenolics in Human Health: Structures, Bioavailability, and Evidence of Protective Effects Against Chronic Diseases", by
Daniele Del Rio, et al., Antioxid Redox Signal. 2013 May 10; 18(14): 1818–1892.

Very poor absorption of plants' poly-phenolic anti-oxidants! From milli-Mole in food down to nano-Mole concentration in the body! Quickly destroyed and eliminated by the body! After decades of hypothesizing and speculations - no direct evidence of health benefits!

Quotes:

...exist in planta, at concentrations in the low-μM-to-mM range. However, after ingestion, dietary (poly)phenolics appear in the circulatory system not as the parent compounds, but as phase II metabolites, and their presence in plasma after dietary intake rarely exceeds nM concentrations. Substantial quantities of both the parent compounds and their metabolites pass to the colon where they are degraded by the action of the local microbiota,
...
Evidence relating to the anticancer effects of (poly)phenols is limited. The majority of available clinical evidence has been with green tea/(poly)phenols in populations at a high risk of cancer development, with results proving inconclusive.
...
While a few of studies suggest that (poly)phenol-rich foods prevent lymphocyte DNA damage, no direct link with a decrease in cancer risk can be established from those studies.
...
As yet, it is too premature to consider the potential use of (poly)phenolic compounds as therapeutic agents.

Updated 22/12/2018

This is probably the main reason why dietary anti-oxidants don't work:

"Antioxidants prevent health-promoting effects of physical exercise in humans"
by Michael Ristow, et. al., PNAS May 26, 2009 106 (21) 8665-8670; March 31, 2009

...We evaluated the effects of a combination of vitamin C (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as measured by glucose infusion rates (GIR) during a hyperinsulinemic, euglycemic clamp in previously untrained (n = 19) and pretrained (n = 20) healthy young men. Before and after a 4 week intervention of physical exercise, GIR was determined, and muscle biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential influences of vitamins on exercise effects. Exercise increased parameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants...
...
Consistent with the concept of mitohormesis, exercise-induced oxidative stress ameliorates insulin resistance and causes an adaptive response promoting endogenous antioxidant defense capacity. Supplementation with antioxidants may preclude these health-promoting effects of exercise in humans.

vegan diet lowers muscle mass and doesn't protect against oxidative damage

.
"Effect of restriction vegan diet's on muscle mass, oxidative status, and myocytes differentiation: A pilot study", Vanacore D. et al., J Cell Physiol. 2018 Dec;233(12) 

Quote:

...we observed a significant decrease in muscle mass index and lean body mass in vegan compared to vegetarian and omnivore groups, and higher serum homocysteine levels in vegetarians and vegans compared to omnivores. ... The results obtained in this study demonstrated that restrictive vegan diet could not prevent the onset of metabolic and cardiovascular diseases nor protect by oxidative damage.

Wiki veganism

vegan diet may make one mentally disabled

.
Being Vegan Makes You Mentally Disabled, Warns Top Danish Doctor

Dr. Allan Lund of Rigshospitalet in Copenhagen highlighted the risks of a vegan lifestyle for young people in an ​appearance last week on Danish TV.

“Such a diet may involve developing different brain symptoms, with muscle weakness, poor contact, and epilepsy,” he told TV4. "And in the long term mental retardation."

According to Lund, his hospital has recently treated a number of vegan kids with such problems.

The news program aired amid a national debate in Denmark over the growing phenomenon of parents putting their children on a plant-based diet.

Wiki: By Ferdous - Own work, CC BY-SA 4.0,

Update 24/12/2018
For adults, also infertility risk and bone fractures:

Food intake diet and sperm characteristics in a blue zone: a Loma Linda Study."

Veganism, vegetarianism, bone mineral density, and fracture risk: a systematic review and meta-analysis

"Save" the World at your own risk, without actually saving anything. All risk (of wiping-out humanity) and no benefit!

low fat low caloric diet may promote gallstones

.

Vegetarians beware!

Gallbladder kinetics in obese patients/Effect of a regular meal and low-calorie meal", Leonardo Marzio et al., January 1988, Vol 33, Issue 1, pp 4–9

Quote:

A low-calorie, low-fat diet augmenting gallbladder volume may favor bile stasis and therefore the likelihood of developing gallstones.

Mitochondrial DNA inherited from both parents!

.

Paper: "Biparental Inheritance of Mitochondrial DNA in Humans", by
Shiyu Luo, et al., PNAS, November 26, 2018


Quote:

The energy-producing organelle mitochondrion contains its own compact genome, which is separate from the nuclear genome. In nearly all mammals, this mitochondrial genome is inherited exclusively from the mother, and transmission of paternal mitochondria or mitochondrial DNA (mtDNA) has not been convincingly demonstrated in humans. In this paper, we have uncovered multiple instances of biparental inheritance of mtDNA spanning three unrelated multiple generation families, a result confirmed by independent sequencing across multiple unrelated laboratories with different methodologies. Surprisingly, this pattern of inheritance appears to be determined in an autosomal dominantlike manner. This paper profoundly alters a widespread belief about mitochondrial inheritance and potentially opens a novel field in mitochondrial medicine.

To reduce nitrates eat less vegetables

.
5 times more dietary nitrates come from vegetables than from cured meats!

Not as bad ...  (Wiki - Saussage)

Not as healthy ...(Wiki Healthy_diet)

"Contribution of vegetables and cured meat to dietary nitrate and nitrite intake in Italian population: Safe level for cured meat and controversial role of vegetables"
Rossana Roila et al., Italian Journal of Food Safety, Vol 7, No 3 (2018)

Paper

Table 1 from the quoted paper.

The paper found that most nitrates in an average diet studied, come from vegetables not cured meats!


Quote:

The average consumption among population resulted 3.45 g/kg bw/die [gram per kg body per daily dietary intake] and 0.62 g/kg bw/die for vegetables and cured meat respectively. The obtained data confirm that nitrate ADI was higher than the limits of 3.7 mg/kg bw/die for infants and was the highest exposure level for people of all ages. Cured meat consumption did not contribute to nitrate ADI exceedance neither as a mean nor as 99th percentile of exposure.

Mediterranean diet is good, adding meat & dairy makes it better!

.
as the following two studies have recently demonstrated:

1) "A Mediterranean-style eating pattern with lean, unprocessed red meat has cardiometabolic benefits for adults who are overweight or obese in a randomized, crossover, controlled feeding trial",
Lauren E O'Connor, Douglas Paddon-Jones, Amy J Wright, Wayne W Campbell,
The American Journal of Clinical Nutrition, Volume 108, Issue 1, 1 July 2018, Pages 33–40

Note: they used lean read meat. I predict a follow-up study titled "A Mediterranean-style eating pattern with fatty, unprocessed red meat has the greatest cardiometabolic benefits"!


2) "A Mediterranean diet supplemented with dairy foods improves markers of cardiovascular risk: results from the MedDairy randomized controlled trial",
Alexandra T Wade, Courtney R Davis, Kathryn A Dyer, Jonathan M Hodgson, Richard J Woodman, Karen J Murphy,
The American Journal of Clinical Nutrition, nqy207, https://doi.org/10.1093/ajcn/nqy207
Published: 22 October 2018


Quote:

Results
Compared with the LF intervention, the MedDairy intervention resulted in a significantly lower morning SBP (mean difference: −1.6 mm Hg; 95% CI: −2.8, −0.4 mm Hg; P = 0.01), lower morning diastolic blood pressure (mean difference: −1.0; 95% CI: −1.7, −0.2 mm Hg; P = 0.01) and clinic SBP (mean difference: −3.5 mm Hg; 95% CI: −6.4, −0.7 mm Hg; P = 0.02), significantly higher HDL cholesterol (mean difference: 0.04 mmol/L; 95% CI: 0.01, 0.06 mmol/L; P < 0.01), lower triglycerides (mean difference: = −0.05 mmol/L; 95% CI: −0.08, −0.01 mmol/L; P < 0.01), and lower ratio of total to HDL cholesterol (mean difference: −0.4; 95% CI: −0.6, −0.2; P < 0.001). No effects were observed for other outcome measures. Conclusions
Following a MedDiet with additional dairy foods led to significant changes in markers of cardiovascular risk over 8 wk. The MedDiet supplemented with dairy may be appropriate for an improvement in cardiovascular risk factors in a population at risk of CVD.

Whole-grain wheat - disproven!

.

The effects of whole-grain compared with refined wheat, rice, and rye on the postprandial blood glucose response: a systematic review and meta-analysis of randomized controlled trials, Kathy Musa-Veloso et al., The American Journal of Clinical Nutrition, Volume 108, Issue 4, 1 October 2018, Pages 759–774,

Quote:

The consumption of ground (wholemeal) wheat, compared with white wheat, was not associated with a significant reduction in blood glucose AUC [Area Under Curve] (−6.7 mmol/L ⋅ min; 95% CI: −25.1, 11.7 mmol/L ⋅ min; P = 0.477). The consumption of wholemeal rye, compared with endosperm rye, was not associated with a significant reduction in blood glucose AUC (−5.5 mmol/L ⋅ min; 95% CI: −24.8, 13.8 mmol/L ⋅ min; P = 0.576). ...

Note: there was some reduction in blood glucose spike (area under curve) following a meal with whole-grain rice versus white rice!

LDL does not cause heart disease

.
Recent paper by Uffe Ravnskov (et al.) - the father of cholesterol "red-pilling"!

"LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature",
Uffe Ravnskov et al., Taylor & Francis Online, 10 Sep 2018


Key issues (quoted):

• The hypothesis that high TC or LDL-C causes atherosclerosis and CVD has been shown to be false by numerous observations and experiments.
• The fact that high LDL-C is beneficial in terms of overall lifespan has been ignored by researchers who support the lipid hypothesis.
• The assertion that statin treatment is beneficial has been kept alive by individuals who have ignored the results from trials with negative outcomes and by using deceptive statistics.
• That statin treatment has many serious side effects has been minimized by individuals who have used a misleading trial design and have ignored reports from independent researchers.
• That high LDL-C is the cause of CVD in FH is questionable because LDL-C does not differ between untreated FH individuals with and without CVD.
• Millions of people all over the world, including many with no history of heart disease, are taking statins, and PCSK-9 inhibitors to lower LDL-C further are now being promoted, despite unproven benefits and serious side effects.
• We suggest that clinicians should abandon the use of statins and PCSK-9 inhibitors, and instead identify and target the actual causes of CVD.

More Quotes (chapter headlines):

2.1 No association between TC and degree of atherosclerosis

2.2 No exposure-response

3.1 An idea supported by fraudulent reviews of the literature

4. Does high LDL-C cause atherosclerosis? 4.1 An idea based on selected patient groups

5.1 LDL-C of patients with acute myocardial infarction is lower than normal

5.2 Elderly people with high LDL-C live the longest

6.1 No exposure-response in the statin trials

6.2 The benefit of statin treatment is exaggerated

6.3 The benefit from statin treatment has been questioned

6.4 Adverse effects from statin treatment

6.5 Does treatment with PCSK-9 inhibitors improve the outcome?
A new cholesterol-lowering drug has recently been introduced. It is an antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK9), which lowers LDL-C by approximately 60%. In FOURIER, the largest and longest PCSK-9 inhibitor trial, Evolocumab was compared with placebo in more than 27,000 statin-treated patients with CVD [92]. The trial was stopped after 2.2 years because the number of MVE was reduced with statistical significance (9.8% vs. 11.3%). However, both CVD mortality and total mortality had increased, although not with statistical significance. A relevant question is therefore, why the trial, the sponsor of which (Amgen) was responsible for data collection, was ended after only 2.2 years. Furthermore, this trial is yet another proof that there is no exposure-response between LDL-C and total or CVD mortality.

7. Does FH prove that high LDL-C causes CVD?

7.1 A low percent of FH [Familial Hypercholesterolemia] individuals die prematurely

7.2 No LDL-C difference between FH individuals with and without CVD

8. Has CVD mortality decreased after the introduction of statin treatment? ...
American National Health and Nutrition Examination Survey [103] found that during the period 1999-2006 the number of AMI and strokes increased from 3.4 to 3.7%, and from 2.0 to 2.9%, respectively. During the same period mean LDL-C level decreased from 126.1 to 114.8 mg/dL, and the self-reported use of lipid-lowering drugs increased from 8 to 13.4%. Furthermore, statin utilization in 12 European countries between 2000 and 2012 was not associated with reduced CHD mortality or its rate of change over the years [104].

9. Conclusion
The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations.

Quoting the captions for the figures!

Figure 2. The association between degree of LDL-C lowering and the absolute risk reduction of total mortality (per cent per year) in 26 statin trials, where total mortality was recorded and which were included in the study by Silverman et al. and in 11 ignored trials. ARR is weakly associated with degree of LDL-C lowering in the included trials (y = 0.28x + 0.06), but inversely associated in the excluded trials (y = - 0.49x - 0.81). Symbols: see figure 1.

According to Ference et al. [3] the most compelling clinical evidence for causality is provided by “the presence of more than 30 randomized cholesterol-lowering trials that consistently demonstrate that reducing LDL-C reduces the risk of CVD events proportional to the absolute reduction in LDL-C.” As previously noted, this is not true exposure-response. Furthermore, in their figure 5A, that illustrates the association, the authors have only included data from12 of the 30 trials they refer to. If all of the trials in table 1 are included, as we have done in figure 3, there is no association between LDL-C lowering and coronary event rate.

Figure 5. The association between the absolute risk reduction of total mortality in 26 statin trials included in the study by Silverman et al. and in 11 ignored trials; and the year where the trial protocols were published. The vertical line indicates the year where the new trial regulations were introduced. [penalizing publication of false results - the new trials show no risk reduction! commented by S.B.]

-------
added 5/10/2018


QJM. 2018 May 1;111(5):319-325. doi: 10.1093/qjmed/hcy043.
A longitudinal 20 years of follow up showed a decrease in the survival of heart failure patients who maintained low LDL cholesterol levels.
Charach G1

Lactobacillus reuteri and anti-aging

.

Interesting:

Stay 40 years old . . . for the next 40, 50, or 60 years?
May 30, 2018 By Dr. William Davis


Making L. reuteri yogurt
April 7, 2018 By Dr. William Davis


Probiotic Microbes Sustain Youthful Serum Testosterone Levels and Testicular Size in Aging Mice
Theofilos Poutahidis,et al., PLoS One. 2014; 9(1)

Fructose-copper connection

.

"The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency", James J. DiNicolantonio, Dennis Mangan, James H. O'Keefe

Quote:

The overconsumption of sugar may be one of the biggest drivers of NAFLD.4 Several factors may be involved in sugar-driven NAFLD, including bacterial translocation from the gut to the liver and advanced glycation end products.8 However, low hepatic copper levels are also implicated in NAFLD; thus sugar consumption can lead to low copper.9 This suggests that the overconsumption of sugar may lead to NAFLD and insulin resistance via hepatic copper deficiency.

In a rat model of NAFLD, dietary sucrose and copper deficiency increased inflammation, fibrosis and lipogenesis.9 Compared to a control diet in which rats were fed with sufficient copper and 10% sucrose, either a high-sucrose diet or a low copper diet increased the hepatic expression of genes regulating inflammation and fibrosis. The low copper diet led to low serum and hepatic copper, increased lipid peroxidation and histopathology similar to that found in NAFLD. The combined low copper and high sugar diet led to all of these changes as well as hepatic insulin resistance and liver damage, but neither low copper nor high sugar caused weight gain. Low copper and high sugar promoted gene expression and physiological processes typical of NAFLD as well as non-alcoholic steatohepatitis (NASH) even without weight gain.

The fructose component of dietary sucrose, in particular, can induce copper deficiency. In rats, a diet of only 3% fructose from beverage intake – a rather modest fructose consumption that is lower than typical intake of Americans – impaired copper status and led to a significant induction of hepatic injury, iron overload and fat accumulation.10 Therefore, fructose-induced copper deficiency could be an important mechanism behind fructose-induced NAFLD. Ultra-high consumption of fructose is not necessarily required for fructose-induced fatty liver with levels lower than the average American consumption capable of inducing it in rats.

Alzheimer and blood glucose

.

Sugar’s “tipping point” link to Alzheimer’s disease revealed

For the first time a “tipping point” molecular link between the blood sugar glucose and Alzheimer’s disease has been established by scientists, who have shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer’s.

Abnormally high blood sugar levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer’s disease is less familiar.

Diabetes patients have an increased risk of developing Alzheimer’s disease compared to healthy individuals. In Alzheimer’s disease abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.


Dr Rob Williams, Dr Omar Kassaar and Prof Jean van den Elsen

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer’s was not understood.

But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King’s College London, have unraveled that link.

By studying brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation, the team discovered that in the early stages of Alzheimer’s glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer’s disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the ‘tipping point’ in disease progression. It appears that as Alzheimer’s progresses, glycation of these enzymes increases.

Reference:

"Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer’s Disease", by
Omar Kassaar et al.

No benefit in LDL-C lowering, trend toward harm.

.



Quote

No beneficial relationship was found between LDL-C lowering and cardiovascular events explored by meta-regression; instead, there was a trend toward harm.

The systematic review ...,Battaggia A, et al. Curr Med Res Opin. 2018.

Quote

CONCLUSIONS: The relationship between LDL-C lowering and cardiovascular events has not showed any significant association (and even a tendency toward harm), challenging the "lower the better" theory. A separate meta-analysis of trials recruiting familial hypercholesterolemia patients has showed a tendency to harm for all outcomes with PCSK9 antibodies. Therefore, at the moment, the data available from randomized trials does not clearly support the use of these antibodies.