Results: Prostate cancer and BPH patients presented higher total, fT and bT levels than CG. IGF-1, insulin and HOMA index were higher in BPH than in the other two groups.
...epidemiological and pathophysiological studies suggest that hyperglycemia may be largely responsible for CVD. Blood glucose has been reported as an independent predictor of atherosclerosis and blood glucose level greater than 90 mg/dl can lead to atherosclerosis in the carotid artery [125]. Long-term follow up data from patients with type 1 and type 2 diabetes suggest that hyperglycemia is a risk factor for diabetes related diseases and CVDMoreover, it has been suggested by Salvin et al. [126] that a 1 unit increase in the total glycosylated hemoglobin or HbA1C, can increase the risk of CVD by up to 18%. Even in the absence of overt diabetes, impairment in the glucose homeostasis can affect the cardiac autonomic function leading to high risk of cardiac diseases [127].
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In this sense, recently it has been shown that cyclic ketone bodies preserve “young cardiac phenotype” in old mice [167]. On the other hand, it has been reported that isocaloric ketogenic diet (very low in carbohydrates and high in fats and/or proteins) increases lifespan [168].
Overall, insulin resistance contributes to generate CVD via two independent pathways: (1) atheroma plaque formation and (2) ventricular hypertrophy and diastolic abnormality.
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| From Wiki Salt |
Abstract
Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium < 20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium > 150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m(2), were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P < .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR [insulin resistance]. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.
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Human longevity is a complex phenotype with a significant familial component, yet little is known about its genetic antecedents. Increasing evidence from animal models suggests that the insulin/IGF-1 signaling (IIS) pathway is an important, evolutionarily conserved biological pathway that influences aging and longevity.
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Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype.
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One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.
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While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.
She made her remarkable breakthrough after studying roundworms, specifically the C.elegans, a worm just a millimetre in size that lives in soil in temperate climates all over the world. By tweaking some of their genes she has been able to help these worms live up to six times longer than normal. 'Not only that, but we also know how to make them stay healthy all that time as well,' she told an audience at the Wellcome Collection in London earlier this month.
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Scientists already knew how to make laboratory animals live longer and healthier lives - you just cut back their calories to about three-quarters of their normal amount. ... But what Professor Kenyon found out was why drastically reducing calories has such a remarkable effect. She discovered that it changed the way two crucial genes behaved. It turned down the gene that controls insulin, which in turn switched on another gene, which acted like an elixir of life. 'We jokingly called the first gene the Grim Reaper because when it’s switched on, the lifespan is fairly short,' she explains. The second 'elixir' gene seems to bring all the anti-ageing benefits - its proper name is DAF 16, but it was quickly nicknamed 'Sweet Sixteen' because it turned the worms into teenagers.
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Discovering the Grim Reaper gene has prompted the professor to dramatically alter her own diet, cutting right back on carbohydrates. That’s because carbs make your body produce more insulin (to mop up the extra blood sugar carbs produce); and more insulin means a more active Grim Reaper. So the vital second gene, the 'elixir' one, won't get turned on.
To test this, last year she added a tiny amount of sugary glucose to the normal diet of some of her worms that had had their genes engineered so they were living much longer, healthier lives. 'The effect was remarkable,' she says. 'The sugary glucose blocked the ''youthful'' genes and they lost most of the health gains.'
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Following Kenyon’s lead, other researchers started looking for the Grim Reaper/ Sweet Sixteen combination in other animals — and of course in humans.
They found it.
One clue came from a small remote community of dwarves living in northern Ecuador who are cancer-free. They are missing the part of the Grim Reaper gene that controls a hormone called insulin-like growth factor. The downside is they only grow to 4ft tall because the hormone is needed for growth. But this missing bit of the Grim Reaper gene also means they don’t develop cancer and are less likely to suffer from heart disease or obesity.
Professor Jeff Holly, who specialises in insulin-like growth factor, confirms that it is linked to cancer of the prostate, breast and colon. In fact raised insulin levels, triggered by high carbohydrate consumption, could be what connects many of our big killers. Research is at its early stage, but raised insulin triggers an increase in cholesterol production in the liver, makes the walls of blood vessels contract so blood pressure goes up and stimulates the release of fats called triglycerides (linked to heart disease).
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'Carbohydrates, and especially refined ones like sugar, make you produce lots of extra insulin. I’ve been keeping my intake really low ever since I discovered this. I've cut out all starch such as potatoes, noodles, rice, bread and pasta. Instead I have salads, but no sweet dressing, lots of olive oil and nuts, tons of green vegetables along with cheese, chicken and eggs. I'll have a hamburger without a bun and fish without batter or chips. I eat some fruit every day, but not too much and almost no processed food. I stay away from sweets, except 80 per cent chocolate.'
