The clock ticks faster.


The signs of physical and functional decline may take a few years to show
APThe signs of physical and functional decline may take a few years to show
Early puberty, hypertension and diabetes in children, early menopause… The alarming issue of premature ageing points inescapably to our way of living, finds out Sudha Umashanker

Girls as young as seven or eight coming of age, young children being diagnosed with hypertension and diabetes, women with plummeting ovarian reserves in their late 20s or early 30s — the ageing clock seems to be ticking differently these days.

Kousalya Nathan, lifestyle and age management consultant, Nova Specialty Surgery, Chennai, points out, “More than ageing and its associated degenerative disorders, the alarming problem is premature ageing, which implies significant functional decline in various organs due to unmanaged lifestyle disorders.”

As the International Journal of Diabetes Care (1999) states, “Although Type 2 Diabetes Mellitus has historically been characterized as an adult onset of diabetes, it has been shown to be on the rise in young people in recent years, comprising some alarming 30 per cent of new cases of diabetes in the second decade of life. The mean age at diagnosis of Type 2 Diabetes in young people is 12-14 years.” (Incidentally, Indian ethnicity is at higher risk.)

Listing out the factors suggestive of the prevalence of premature ageing, Dr. Nathan notes, “Early puberty is a pointer. We also live in an environment that favours unhealthy weight gain in children and adolescents. This has reached epidemic proportions in India, with consequences ranging from inability to play or climb stairs, to hypertension, dyslipidemia, back pain and psychosocial problems. Even greying and loss of skin tone, which are signs of middle age, are seen in 10- to 12-year-olds. In the worst-case scenario, deaths due to non-communicable diseases in those in their 30s and 40s are also happening.”

Nandita Palshetkar, infertility specialist, Lilavati Hospitals Mumbai and Fortis Bloom IVF Centres, says, “Nowadays, more and more girls are attaining early puberty. Earlier, puberty which was seen at age 12 is now seen at the age of seven to eight years, in approximately 15 per cent of the girls. There are several reasons for this — such as unhealthy weight gain, stress, estrogens-like hormones such as bisphenol A found in hard plastics, certain metals that act as metalloestrogens, (eg. tin, cadmium, mercury, lead and aluminium, copper), situations in which the father is absent or the child is living with the step-father, Vitamin D deficiency, early exposure to sex-related messages in the media etc. Higher body mass index is associated most often with lifestyle changes that have occurred in the last couple of decades in our society. Early puberty, in turn, is associated with repercussions such as increased risk of heart problem, osteoporosis and early menopause.”

Rapid depletion of ovarian reserves, and therefore early ovarian ageing in young women, is yet another cause of concern. While it could be due to polycystic ovaries, in several cases, the cause is unknown. “Measures must be taken to reduce contamination by Endocrine Disrupting Compounds (EDCs) if we want to take steps to decrease reproductive disorders in women of the next generation,” stresses Dr. Palshetkar. EDCs that affect the functioning of the thyroid and ovary are found in pesticides, dioxins (produced when plastic is burnt, certain industrial processes and from improper incineration of waste), bisphenols (found in hard plastics, some baby bottles, water bottles and the insides of some food and beverage cans.) Corroborating the incidence of diabetes in overweight young children, Vijay Viswanathan, head and chief diabetologist, M.V. Hospital for Diabetes, Chennai, says that a recent survey in Chennai done by his institution showed that “many children who were overweight had raised blood pressure levels. These children showed aspects of insulin resistance, which makes them prone to hypertension and also diabetes.”

Asked if this can be considered a form of ageing, Dr. Viswanathan affirms, “Yes, this is a type of ageing, since the blood vessels develop stiffness and lose their elasticity even by the age of 10 or 15 in children who are insulin-resistant. These early blood vessel changes make these children prone to developing hypertension at an early stage, and may also lead to heart blocks by the time they get into their 20s or 30s.”

What are the signs that should alert us before visible changes of ageing happen?

Weight gain, skin discoloration in underarms, inner thighs, nape of the neck, frequent infections, tiredness, irregular periods in girls, rough skin, overeating and eating disorders, stress and sleeping difficulties in children,” should put us on the alert, says Dr. Nathan.

While there are molecular-level changes of ageing in children, to see the physical and functional decline, it might take a few years. “It is a complex and multi-factorial process. Lifestyle accelerates loss of genetic materials, causing premature ageing,” Dr. Nathan concludes.

Preventive steps

Lifestyle modification is top priority.

– Opt for an anti-ageing diet — 60 per cent complex carbohydrates (legumes, cereals and vegetables), 20 per cent protein (white meat, dal, paneer, tofu, soy protein), 20 per cent fats (nuts, olives, sesame seeds, pumpkin seeds)

– Undertake regular physical activity

– Avoid exposure to estrogens-like compounds and environmental toxins

– Consume organically-grown vegetables

– Teach children to bust emotional stress by taking up creative pursuits

 

The clock ticks faster.


The signs of physical and functional decline may take a few years to show
AP The signs of physical and functional decline may take a few years to show
TOPICS

Early puberty, hypertension and diabetes in children, early menopause… The alarming issue of premature ageing points inescapably to our way of living, finds out Sudha Umashanker

Girls as young as seven or eight coming of age, young children being diagnosed with hypertension and diabetes, women with plummeting ovarian reserves in their late 20s or early 30s — the ageing clock seems to be ticking differently these days.

Kousalya Nathan, lifestyle and age management consultant, Nova Specialty Surgery, Chennai, points out, “More than ageing and its associated degenerative disorders, the alarming problem is premature ageing, which implies significant functional decline in various organs due to unmanaged lifestyle disorders.”

As the International Journal of Diabetes Care (1999) states, “Although Type 2 Diabetes Mellitus has historically been characterized as an adult onset of diabetes, it has been shown to be on the rise in young people in recent years, comprising some alarming 30 per cent of new cases of diabetes in the second decade of life. The mean age at diagnosis of Type 2 Diabetes in young people is 12-14 years.” (Incidentally, Indian ethnicity is at higher risk.)

Listing out the factors suggestive of the prevalence of premature ageing, Dr. Nathan notes, “Early puberty is a pointer. We also live in an environment that favours unhealthy weight gain in children and adolescents. This has reached epidemic proportions in India, with consequences ranging from inability to play or climb stairs, to hypertension, dyslipidemia, back pain and psychosocial problems. Even greying and loss of skin tone, which are signs of middle age, are seen in 10- to 12-year-olds. In the worst-case scenario, deaths due to non-communicable diseases in those in their 30s and 40s are also happening.”

Nandita Palshetkar, infertility specialist, Lilavati Hospitals Mumbai and Fortis Bloom IVF Centres, says, “Nowadays, more and more girls are attaining early puberty. Earlier, puberty which was seen at age 12 is now seen at the age of seven to eight years, in approximately 15 per cent of the girls. There are several reasons for this — such as unhealthy weight gain, stress, estrogens-like hormones such as bisphenol A found in hard plastics, certain metals that act as metalloestrogens, (eg. tin, cadmium, mercury, lead and aluminium, copper), situations in which the father is absent or the child is living with the step-father, Vitamin D deficiency, early exposure to sex-related messages in the media etc. Higher body mass index is associated most often with lifestyle changes that have occurred in the last couple of decades in our society. Early puberty, in turn, is associated with repercussions such as increased risk of heart problem, osteoporosis and early menopause.”

Rapid depletion of ovarian reserves, and therefore early ovarian ageing in young women, is yet another cause of concern. While it could be due to polycystic ovaries, in several cases, the cause is unknown. “Measures must be taken to reduce contamination by Endocrine Disrupting Compounds (EDCs) if we want to take steps to decrease reproductive disorders in women of the next generation,” stresses Dr. Palshetkar. EDCs that affect the functioning of the thyroid and ovary are found in pesticides, dioxins (produced when plastic is burnt, certain industrial processes and from improper incineration of waste), bisphenols (found in hard plastics, some baby bottles, water bottles and the insides of some food and beverage cans.) Corroborating the incidence of diabetes in overweight young children, Vijay Viswanathan, head and chief diabetologist, M.V. Hospital for Diabetes, Chennai, says that a recent survey in Chennai done by his institution showed that “many children who were overweight had raised blood pressure levels. These children showed aspects of insulin resistance, which makes them prone to hypertension and also diabetes.”

Asked if this can be considered a form of ageing, Dr. Viswanathan affirms, “Yes, this is a type of ageing, since the blood vessels develop stiffness and lose their elasticity even by the age of 10 or 15 in children who are insulin-resistant. These early blood vessel changes make these children prone to developing hypertension at an early stage, and may also lead to heart blocks by the time they get into their 20s or 30s.”

What are the signs that should alert us before visible changes of ageing happen?

Weight gain, skin discoloration in underarms, inner thighs, nape of the neck, frequent infections, tiredness, irregular periods in girls, rough skin, overeating and eating disorders, stress and sleeping difficulties in children,” should put us on the alert, says Dr. Nathan.

While there are molecular-level changes of ageing in children, to see the physical and functional decline, it might take a few years. “It is a complex and multi-factorial process. Lifestyle accelerates loss of genetic materials, causing premature ageing,” Dr. Nathan concludes.

Preventive steps

Lifestyle modification is top priority.

– Opt for an anti-ageing diet — 60 per cent complex carbohydrates (legumes, cereals and vegetables), 20 per cent protein (white meat, dal, paneer, tofu, soy protein), 20 per cent fats (nuts, olives, sesame seeds, pumpkin seeds)

– Undertake regular physical activity

– Avoid exposure to estrogens-like compounds and environmental toxins

– Consume organically-grown vegetables

– Teach children to bust emotional stress by taking up creative pursuits

Are Alzheimer’s and diabetes the same disease?


HAVING type 2 diabetes may mean you are already on the path to Alzheimer’s. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer’s.

“Perhaps you should use Alzheimer’s drugs at the diabetes stage to prevent cognitive impairment in the first place,” says Ewan McNay from the University at Albany in New York.

Alzheimer’s cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion.

Are brain changes associated with Alzheimer's (green) reversible? <i>(Image: Medical Body Scans/Jessica Wilson/Photo Researchers/SPL)</i>

In 2005, a study by Susanne de la Monte’s group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer’s. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be “diabetic” but so it seemed, could your brain.

Feeding animals a diet designed to give them type 2 diabetes leaves their brains riddled with insoluble plaques of a protein called beta-amyloid – one of the calling cards of Alzheimer’s. We also know that insulin plays a key role in memory. Taken together, the findings suggest that Alzheimer’s might be caused by a type of brain diabetes.

If that is the case, the memory problems that often accompany type 2 diabetes may in fact be early-stage Alzheimer’s rather than mere cognitive decline.

Although there is no definitive consensus on the exact causes of Alzheimer’s, we do know that brains get clogged with beta-amyloid plaques. One idea gaining ground is that it is not the plaques themselves that cause the symptoms, but their precursors – small, soluble clumps of beta-amyloid called oligomersMovie Camera. The insoluble plaques could actually be the brain’s way of trying to isolate the toxic oligomers.

To investigate whether beta-amyloid might also be a cause of cognitive decline in type 2 diabetes, McNay, Danielle Osborne and their colleagues fed 20 rats a high-fat diet to give them type 2 diabetes. These rats, and another 20 on a healthy diet, were then trained to associate a dark cage with an electric shock. Whenever the rats were returned to this dark cage, they froze in fear – measuring how long they stayed still is a standard way of inferring how good their memory is.

Memory boost

As expected, the diabetic rats had weaker memories than the healthy ones – they froze in the dark for less than half the time of their healthy counterparts. To figure out whether this was due to the beta-amyloid plaques or the soluble precursors, Pete Tessier at the Rensselaer Polytechnic Institute in Troy, New York, engineered fragments of antibodies that disrupt the action of one or the other.

When the plaque-disrupting antibodies were injected into diabetic rats, no change was seen. However, after receiving antibodies specific for oligomers, they froze for just as long as the healthy rats. “The cognitive deficit brought on by their diabetes is entirely reversed,” says McNay.

Until now, the standard explanation for the cognitive decline associated with type 2 diabetes is that it is a result of insulin signalling gone awry. One effect is to reduce the hippocampus’s ability to transport energy, or glucose, to neurons during a cognitive task. The fact that amyloid builds up in the brains of diabetic animals – and also in people, was seen as an unhappy consequence of insulin imbalance.

These experiments suggest oligomers are actually to blame. Previous work from other groups has shown that the same enzymes break down both insulin and beta-amyloid oligomers – and that the oligomers prevent insulin binding to its receptors in the hippocampus. So when there is too much insulin around – as there is in someone with type 2 diabetes – those enzymes are working flat out to break it down. This preferential treatment of insulin leaves the oligomers to form clumps, which then keep insulin from its receptors, causing a vicious spiral of impaired brain insulin signalling coupled with cognitive decline.

“We think that our treatment soaked up the amyloid oligomers, so that they could no longer block insulin from binding to its receptors,” says McNay, who presented the preliminary data at the Society for Neuroscience meeting in San Diego earlier this month. “Everyone thinks of amyloid build-up as a consequence of the events that cause cognitive impairment in diabetes, but we’re saying it’s actually a cause.” It means, he says, that the cognitive decline seen in type 2 diabetes may be thought of as early-stage Alzheimer’s.

It’s a bold claim, and if correct, one with big implications. Given that the number of people with type 2 diabetes is expected to jump from 382 million now to 592 million by 2035, we might expect to see a similar trajectory for associated Alzheimer’s (New Scientist, 1 September 2012). If beta-amyloid build-up can be stopped in people with type 2 diabetes and their cognitive impairment reversed – perhaps many of them will never progress to Alzheimer’s.

For the last few years, organisations like the UK’s Alzheimer’s Society have been backing clinical trials to look for diabetes drugs that may have an effect on Alzheimer’s patients. “We’re saying that this may be not the only way to think about it,” says McNay.

The next step is to repeat the work, and if the results are corroborated, start looking for a drug that would do the same thing as the group’s modified antibodies, without having to inject the drug directly into the hippocampus. It will also be necessary to work out just how much amyloid the brain can safely do without, since low levels are important for memory formation.

“The work opens the door to inoculating the most at risk group, people with type 2 diabetes,” says Tres Thompson of the University of Texas at Dallas. There have been plenty of failed attempts to use antibodies to relieve Alzheimer’s in the past. “But these were all in people with advanced stages of the disease. Vaccinating people much earlier could give better results.”

Some researchers are still wary of focusing on beta-amyloid when 20 years of working on a treatment for that particular aspect of the disease has come to nothing. “I think it’s brilliant work – he’s using new techniques that seem to be working, but it’s still very beta-centric,” says Olivier Thibault at the University of Kentucky in Lexington. He cautiously agrees that McNay’s data do seem to suggest a causative link between beta-amyloid and impaired insulin signalling but says the group needs to factor in the effect of ageing – both diabetes and Alzheimer’s become more likely as we grow older.

Jessica Smith, spokeswoman for the UK Alzheimer’s Society in London welcomes the work. “We need to tease out the difference between those with type 2 diabetes who develop Alzheimer’s and those who don’t. If people were developing the signs earlier than we thought, then perhaps we can intervene earlier, rather than waiting until they have full clinical Alzheimer’s.”

Of course, there is another solution to staving off type 2 diabetes and any consequential Alzheimer’s that requires no drugs at all. “Go to the gym and eat fewer twinkies,” says McNay.

Brain may play key role in blood sugar metabolism and diabetes development.


A growing body of evidence suggests that the brain plays a key role in glucose regulation and the development of type 2 diabetes, researchers write in the Nov. 7 ssue of the journal Nature. If the hypothesis is correct, it may open the door to entirely new ways to prevent and treat this disease, which is projected to affect one in three adults in the United States by 2050.

In the paper, lead author Dr. Michael W. Schwartz, UW professor of medicine and director of the Diabetes and Obesity Center of Excellence, and his colleagues from the universities of Cincinnati, Michigan, and Munich,  note that the brain was originally thought to play an important role in maintaining normal glucose metabolism  With the discovery of insulin in the 1920s, the focus of research and diabetes care shifted to almost exclusively to insulin. Today, almost all treatments for diabetes seek to either increase insulin levels or increase the body’s sensitivity to insulin.

“These drugs,” the researchers write, “enjoy wide use and are effective in controlling hyperglycemia [high blood sugar levels], the hallmark of type 2 diabetes, but they address the consequence of diabetes more than the underlying causes, and thus control rather than cure the disease.”

New research, they write, suggests that normal glucose regulation depends on a partnership between the insulin-producing cells of the pancreas, the pancreatic islet cells, and neuronal circuits in the hypothalamus and other brain areas that are intimately involved in maintaining normal glucose levels. The development of diabetes type 2, the authors argue, requires a failure of both the islet-cell system and this brain-centered system for regulating blood sugar levels .

In their paper, the researchers review both animal and human studies that indicate the powerful effect this brain-centered regulatory system has on blood glucose levels independent of the action of insulin. One such mechanism by which the system promotes glucose uptake by tissues is by stimulating what is called “glucose effectiveness.” As this process accounts for almost 50 percent of normal glucose uptake, it rivals the impact of insulin-dependent mechanisms driven by the islet cells in the pancreas.

The findings lead the researchers to propose a two-system model of regulating blood sugar levels composed of the islet-cell system, which responds to a rise in glucose levels by primarily by releasing insulin, and the brain-centered system that enhances insulin-mediated glucose metabolism while also stimulating glucose effectiveness.

The development of type 2 diabetes appears to involve the failure of both systems, the researchers say. Impairment of the brain-centered system is common, and it places an increased burden on the islet-centered system. For a time, the islet-centered system can compensate, but if it begins to fail, the brain-centered system may decompensate further, causing a vicious cycle that ends in diabetes.

Boosting insulin levels alone will lower glucose levels, but only addresses half the problem. To restore normal glucose regulation requires addressing the failures of the brain-centered system as well. Approaches that target both systems may not only achieve better blood glucose control, but could actually cause diabetes to go into remission, they write.

Measuring Blood Sugar With Light.


Technology designed in Germany may help people with Type 1 and Type 2 diabetes; described in Review of Scientific Instruments

WASHINGTON D.C. October 25, 2013 — One of the keys to healthful living with Type 1 and Type 2 diabetes is monitoring blood glucose (sugar) levels to ensure they remain at stable levels. People can easily and reliably do this at home using electronic devices that read sugar levels in a tiny drop of blood.

Now a team of German researchers has devised a novel, non-invasive way to make monitoring easier. Using infrared laser light applied on top of the skin, they measure sugar levels in the fluid in and under skin cells to read blood sugar levels. They describe their method in the current edition of Review of Scientific Instruments, which is produced by AIP Publishing.

“This opens the fantastic possibility that diabetes patients might be able to measure their glucose level without pricking and without test strips,” said lead researcher, Werner Mäntele, Ph.D. of Frankfurt’s Institut für Biophysik, Johann Wolfgang Goethe-Universität.

“Our goal is to devise an easier, more reliable and in the long-run, cheaper way to monitor blood glucose,” he added.

The “Sweet Melody” of Glucose

Their new optical approach uses photoacoustic spectroscopy (PAS) to measure glucose by its mid-infrared absorption of light. A painless pulse of laser light applied externally to the skin is absorbed by glucose molecules and creates a measurable sound signature that Dr. Mäntele’s team refers to as “the sweet melody of glucose.” This signal enables researchers to detect glucose in skin fluids in seconds.

The data showing the skin cell glucose levels at one-hundredth of a millimeter beneath the skin is related to blood glucose levels, Mäntele said, but previous attempts to use PAS in this manner have been hampered by distortion related to changes of air pressure, temperature and humidity caused by the contact with living skin.

To overcome these constraints, the team devised a design innovation of an open, windowless cell architecture. While it is still experimental and would have to be tested and approved by regulatory agencies before becoming commercially available, the team continues to refine it.

Blood sugar levels could be linked to memory loss in people without diabetes – Mirror.co.uk


Journal study finds with with lower blood sugar levels achieved highest scores in memory tests – those with high levels could suffer memory loss

People who have even slightly raised blood sugar levels may suffer memory loss, a study shows.

Researchers performed tests on 141 healthy people with an average age of 63.

None had diabetes or pre-diabetic symptoms.

But the study published in journal Neurology found those with with lower blood sugar levels achieved better scores in memory tests.

In a test to recall 15 words 30 minutes after hearing them, higher blood sugar levels were linked with poorer memory.

Lead researcher Dr Agnes Floel, of the Charite University Medicine in Berlin, Germany, said: “These results suggest that even for people within the normal range of blood sugar, lowering their blood sugar levels could be a promising strategy for preventing memory problems and cognitive decline as they age.

“Strategies such as lowering calorie intake and increasing physical activity should be tested.”

Dr Clare Walton, of the Alzheimer’s Society, said: “We already know that Type 2 diabetes is a risk factor for developing Alzheimer’s disease but this new study suggests that higher blood sugar levels may also be linked to poor memory in people without diabetes.

“The research suggests that regulating blood sugar levels might be a way to improve people’s memory, even if they don’t have diabetes.”

Dr Simon Ridley, of Alzheimer’s Research UK, added: “While we do not know whether the people in this study would have gone on to develop dementia, the findings serve as a warning that we should be conscious of the impact that subtle changes in our health could have on our brain.

“Current evidence suggests the best way to keep the brain healthy is to eat a balanced diet, take regular exercise, maintain a healthy weight, not smoke and keep blood pressure and cholesterol levels in check.”

Effects of Sulfonylureas on Tumor Growth.


Type 2 diabetes mellitus patients are at higher cancer risk, probably because of hyperinsulinemia and insulin growth factor 1 pathway activation. The effects of antidiabetic drugs on cancer risk have been described and discussed in several studies suggesting opposite effects of the biguanide metformin and sulfonylureas on cancer incidence and mortality. The anticancer mechanisms of metformin have been clarified, and some clinical studies, particularly in breast cancer patients, have been published or are currently ongoing; however, data about the effects of sulfonylureas on cancer growth are less consistent. The aims of this work are to review preclinical evidence of second-generation sulfonylureas effects on tumor growth, to clarify the potential mechanisms of action, and to identify possible metabolic targets for patient selection. Most evidence is on the adenosine triphosphate-sensitive potassium channels inhibitor glibenclamide, which interacts with reactive oxygen species production thus inducing cancer cell death. Among diarylsulfonylureas, next-generation DW2282 derivatives are particularly promising because of the proapoptotic activity in multidrug-resistant cells.

 

Source: The Oncologist.

 

This is why high fructose corn syrup is dangerous.


High Fructose Corn Syrup, also known as HFCS, glucosefructose syrup, glucose syrup, fructose syrup, glucose/fructose, high-fructose maize syrup or corn sugar is a corn-based sweetener that is used in thousands of food products including sodas, soft drinks, fruit juices, ice cream, candy, baked goods, cookies, ketchup, soups, salad dressings, breads, crackers, etc.

HFCS is a mixture of fructose and glucose, and is used by food companies because it is cheaper than sugar and gives food products a longer shelf life.

HFCS is responsible for a host of health problems such as obesity, high cholesterol, insulin problems, Type 2 diabetes, liver damage, hypertension, high blood pressure, heart disease, cancer, migraines, ADHD, etc.
HFCS is often contaminated with mercury which can lead to brain damage.

Here is a great video about the dangers of HFCS:

Corn, the source of high fructose corn syrup, is now often genetically modified, which causes many serious health problems.

Glucose is used as fuel and metabolized by the cells in the body. In contrast, fructose can only be metabolized by the liver which turns fructose into fat. When consuming fructose, 30% will be stored as fat… Fructose, in contrast to glucose, has no effect on appetite, which results in overeating and obesity.

The fructose found in fruit and in some vegetables is actually quite healthy as it contains fiber, vitamins, minerals, enzymes and beneficial phytonutrients. In contrast, the fructose found in HFCS contains no nutrition and actually pulls nutrients from the body! HFCS hinders the absorption of minerals such as magnesium, copper and chromium and affects the receptors of insulin, leading to Type 2 diabetes. In addition, HFCS causes high cholesterol and impairs the immune system.

The food industry is trying to convince us that High Fructose Corn Syrup is natural, equal to sugar and therefore perfectly safe.

Do no longer believe the lies of the food industry and the ‘mainstream’ media. Contrary to what so-called ‘health experts’ claim, HFCS is not safe!

Avoid HFCS for 60 days and discover how your health will improve dramatically!

Other forms of fructose to avoid: crystalline fructose, chicory, inulin, iso glucose and Agave syrup, a highly processed sweetener that is nearly all-fructose.

Also avoid energy and sports drinks because they are loaded with sugar, chemical additives and artificial sweeteners.

Healthier HFCS alternatives:
Organic raw cane sugar, maple syrup, coconut nectar, palm sugar, raw honey and Stevia, the low calorie, all natural sweetener used in Paraguay for centuries.

Source: rawforbeauty.com

 

Anti-depressants’ ‘link to diabetes’


People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers.

The University of Southampton team looked at available medical studies and found evidence the two were linked.

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But there was no proof that one necessarily caused the other.

It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal.

Or the drugs themselves may interfere with blood sugar control.

 “Start Quote

These findings fall short of being strong evidence that taking anti-depressants directly increases risk of type 2 diabetes”

Dr Matthew Hobbs of Diabetes UK

Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk.

Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings.

And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs.

With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say.

Prof Holt said: “Some of this may be coincidence but there’s a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes.

“We need to think about screening and look at means to reduce that risk.”

Diabetes is easy to diagnose with a blood test, and Prof Holt says this ought to be part of a doctor’s consultation.

“Diabetes is potentially preventable by changing your diet and being more physically active.

“Physical activity is also good for your mental health so there’s a double reason to be thinking about lifestyle changes.”

Around three million people in the UK are thought to have diabetes, with most cases being type 2.

Dr Matthew Hobbs of Diabetes UK, said: “These findings fall short of being strong evidence that taking anti-depressants directly increases risk of type 2 diabetes. In this review, even the studies that did suggest a link showed only a small effect and just because two things tend to occur together, it doesn’t necessarily mean that one is causing the other.

“But what is clear is that some anti-depressants lead to weight gain and that putting on weight increases risk of type 2 diabetes. Anyone who is currently taking, or considering taking, anti-depressants and is concerned about this should discuss their concerns with their GP.”

Source: BBC

Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies.


Abstract

Objective To determine whether individual fruits are differentially associated with risk of type 2 diabetes.

Design Prospective longitudinal cohort study.

Setting Health professionals in the United States.

Participants 66 105 women from the Nurses’ Health Study (1984-2008), 85 104 women from the Nurses’ Health Study II (1991-2009), and 36 173 men from the Health Professionals Follow-up Study (1986-2008) who were free of major chronic diseases at baseline in these studies.

Main outcome measure Incident cases of type 2 diabetes, identified through self report and confirmed by supplementary questionnaires.

Results During 3 464 641 person years of follow-up, 12 198 participants developed type 2 diabetes. After adjustment for personal, lifestyle, and dietary risk factors of diabetes, the pooled hazard ratio of type 2 diabetes for every three servings/week of total whole fruit consumption was 0.98 (95% confidence interval 0.96 to 0.99). With mutual adjustment of individual fruits, the pooled hazard ratios of type 2 diabetes for every three servings/week were 0.74 (0.66 to 0.83) for blueberries, 0.88 (0.83 to 0.93) for grapes and raisins, 0.89 (0.79 to 1.01) for prunes, 0.93 (0.90 to 0.96) for apples and pears, 0.95 (0.91 to 0.98) for bananas, 0.95 (0.91 to 0.99) for grapefruit, 0.97 (0.92 to 1.02) for peaches, plums, and apricots, 0.99 (0.95 to 1.03) for oranges, 1.03 (0.96 to 1.10) for strawberries, and 1.10 (1.02 to 1.18) for cantaloupe. The pooled hazard ratio for the same increment in fruit juice consumption was 1.08 (1.05 to 1.11). The associations with risk of type 2 diabetes differed significantly among individual fruits (P<0.001 in all cohorts).

Conclusion Our findings suggest the presence of heterogeneity in the associations between individual fruit consumption and risk of type 2 diabetes. Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, is significantly associated with a lower risk of type 2 diabetes, whereas greater consumption of fruit juice is associated with a higher risk.

Discussion

In three prospective cohorts of US men and women, we found that the associations with risk of type 2 diabetes differed significantly among individual fruits: greater consumption of blueberries, grapes, apples, bananas, and grapefruit were significantly associated with a reduced risk of type 2 diabetes. Most of these associations were quite consistent among three cohorts. Additionally, differences in the glycemic index/glycemic load values of fruits did not account for the association of specific fruits with risk of type 2 diabetes. Moreover, greater fruit juice consumption was associated with an increased risk, and substitution of whole fruits for fruit juice was associated with a lower risk, except for strawberries and cantaloupe.

Results in relation to other studies

In eight previous prospective studies, the association between total fruit consumption and risk of type 2 diabetes was examined,2 3 4 5 6 7 8 9 and the results were mixed. Similar to previous analyses in the Nurses’ Health Study3 and the Finnish Mobile Clinic Health Examination Survey study,2 the current findings supported an inverse association between total fruit consumption and risk of type 2 diabetes, but not in other studies.4 5 6 7 8 9 In contrast to total fruit consumption, evidence on consumption of individual fruits or fruit groups with risk of type 2 diabetes is limited and incomplete. In four prospective studies, consumption of citrus fruit was not associated with a lower risk of type 2 diabetes.5 6 7 8 Apple consumption was inversely associated with risk in the Women’s Health Study29 and in the Finnish study,30 but not in the Iowa Women’s Health Study.31 In addition, greater consumption of berries was associated with a lower risk in the Finnish study,2 but not in the Iowa Women’s Health Study.31 In our previous analyses that focused on anthocyanin rich fruits, intakes of blueberries, strawberries, and apples were associated with a lower risk of type 2 diabetes.32 Consistently, in a clinical trial, increased consumption of berries improved glycemic control among people with diabetes.33 Our current investigation extended the evidence in this regard and found novel, inverse associations for grapes, bananas, and grapefruit.

The different associations of individual fruits with diabetes risk may be due to the heterogeneous composition of these foods. Firstly, blueberries, apples, and red or black grapes contain high levels of anthocyanins.12 In mice with diabetes, bilberry extract rich in anthocyanins can activate adenosine monophosphate-activated protein kinase, enhance glucose uptake and utilization in white adipose tissue and skeletal muscle, and reduce glucose production in the liver.34 Our previous analyses also showed that levels of anthocyanin intake were inversely associated with risk of type 2 diabetes.32 In the current study, further adjustment for anthocyanins did not substantially change the associations for individual fruits, suggesting that the inverse associations of individual fruits are likely due to other constituents of these foods. Both red and white grapes contain high levels of resveratrol in skin.35 In mice, a high fat diet with 0.04% resveratrol increased insulin sensitivity at 24 months compared with the same diet without resveratrol.36 However, randomized controlled trials examining the effects of supplementation of resveratrol on glucose metabolism have generated inconsistent results.37 38 39 Prunes, peaches, plums, apricots, and apples contain chlorogenic acid,40 41 42 43 which may potentially mediate the beneficial effects of coffee consumption on diabetes risk.44 In rats, chlorogenic acid reduces glucose dependent insulinotropic peptide secretion by slowing glucose absorption in the intestine.45Moreover, chlorogenic acid increases muscle glucose uptake in mice with diabetes.46Finally, grapefruits contain high amounts of naringin.12 In rats, naringin inhibits dipeptidyl peptidase 4 similarly to sitagliptin, a dipeptidyl peptidase 4 inhibitor used for the treatment of diabetes.47 Inhibition of dipeptidyl peptidase 4 increases glucagon-like peptide 1, which subsequently leads to improved glucose tolerance.48 In contrast to these specific fruits mentioned above, cantaloupe was associated with an increased risk of type 2 diabetes in the current analysis. Melons have lower levels of phytochemicals than the aforementioned fruits.12 None the less, little evidence exists regarding the effects of melons on glucose metabolism. Although other fruits may also be beneficial for glucose metabolism, significant associations between other specific fruits and risk of type 2 diabetes were not found in the current and previous investigations.5 6 7 8

The glycemic index/glycemic load values of fruits did not seem to be the factor that determined their association with type 2 diabetes in the current study, although in a clinical trial, increased consumption of low glycemic index fruits improved glycemic control among people with diabetes.33 In recent meta-analyses, a higher dietary glycemic index/glycemic load was associated with a greater risk of type 2 diabetes.4950 In the Nurses’ Health Study and Health Professionals Follow-up Study, the associations between dietary glycemic index and risk of type 2 diabetes were positive, although the associations for dietary glycemic load were not significant.51 52 53 None the less, the contribution of total fruit consumption to dietary glycemic load was rather small (about 10%) in these populations. Of individual fruits, the top three contributors to dietary glycemic load were bananas (3-4%), apples (2%), and grapes (1%). In contrast, the relatively high glycemic load values of fruit juices13 along with reduced levels of beneficial nutrients through juicing processes11 12 (for example, the glycemic load values per serving are 6.2 for raw oranges and 13.4 for orange juice, and fibre levels per serving are 3.1 g and 0.5 g, respectively) may explain the positive associations between fruit juice consumption and risk of type 2 diabetes. Moreover, the difference in the viscosity of foods is also an important factor affecting postprandial blood glucose dynamics. Fluids pass through the stomach to the intestine more rapidly than solids even if nutritional content is similar.54 For example, fruit juices lead to more rapid and larger changes in serum levels of glucose and insulin than whole fruits.55 56 Although these mechanisms may potentially explain the diverse associations for individual fruits, further research is apparently needed to confirm our findings on specific fruits in relation to type 2 diabetes and to further elucidate underlying mechanisms.

Strengths and limitations of this study

The present study has several limitations. Firstly, measurement errors were inevitable in the estimates of fruit consumption, especially for individual fruits with lower consumption levels.17 18 Adjustment for energy intake and use of cumulatively averaged intake levels can reduce the magnitude of measurement errors to some extent.26 Generally, random errors in exposure assessments attenuate true associations toward the null. Secondly, the possibility of false positive findings may exist because we examined the associations of multiple fruits in the current investigation without adjusting for multiple comparisons based on a priori hypotheses. Meanwhile, most associations were consistent across three cohorts, and the associations for blueberries, grapes, and apples remained statistically significant even after applying the Bonferroni correction, a conservative method correcting for multiple comparisons. Thirdly, in our food frequency questionnaires, intakes of some individual fruits (apples and pears; peaches, plums, and apricots) were combined because these fruits have similar nutrient profiles. Therefore we could not determine whether the associations for these combined fruits can be ascribed to a specific individual fruit. Fourthly, we cannot exclude the possibility of recall bias in the assessments of diet based on the food frequency questionnaires. However, the prospective study design and exclusion of participants with chronic diseases at baseline should minimize such bias. Fifthly, although in the multivariable analysis we considered a multitude of lifestyle and dietary factors, including other individual fruits, residual or unmeasured confounding may still exist. Finally, our study populations primarily consist of health professionals with European ancestry. Thus our findings may not be generalized to other populations.

Conclusions

Our findings suggest that there is significant heterogeneity in the associations between individual fruits and risk of type 2 diabetes. Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, was significantly associated with a lower risk of type 2 diabetes, whereas greater fruit juice consumption was associated with a higher risk. The differences in the associations between individual fruits were not accounted for by variation in the glycemic index/glycemic load values of individual fruits. Overall, these results support recommendations on increasing consumption of a variety of whole fruits, especially blueberries, grapes, and apples, as a measure for diabetes prevention.

What is already known on this topic

  • Total fruit consumption is not consistently associated with a lower risk of type 2 diabetes
  • The possible heterogeneity among individual fruits regarding the associations with risk of type 2 diabetes has not been examined
  • The associations with risk of type 2 diabetes are different among individual fruits
  • Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, is significantly associated with a lower risk of type 2 diabetes, whereas increased consumption of fruit juices has the opposite association
  • In addition, the associations of individual fruits are not determined by their glycemic index or glycemic load values

What this study adds

 

 

Source: BMJ