The DHA-deprived rats also developed signs of resistance to insulin, a hormone that controls blood sugar and regulates synaptic function in the brain. A closer look at the rats' brain tissue suggested that insulin had lost much of its power to influence the brain cells.

"Because insulin can penetrate the blood–brain barrier, the hormone may signal neurons to trigger reactions that disrupt learning and cause memory loss," Gomez-Pinilla said.

He suspects that fructose is the culprit behind the DHA-deficient rats' brain dysfunction. Eating too much fructose could block insulin's ability to regulate how cells use and store sugar for the energy required for processing thoughts and emotions.

"Insulin is important in the body for controlling blood sugar, but it may play a different role in the brain, where insulin appears to disturb memory and learning," he said. "Our study shows that a high-fructose diet harms the brain as well as the body. This is something new."

Gomez-Pinilla, a native of Chile and an exercise enthusiast who practices what he preaches, advises people to keep fructose intake to a minimum and swap sugary desserts for fresh berries and Greek yogurt, which he keeps within arm's reach in a small refrigerator in his office. An occasional bar of dark chocolate that hasn't been processed with a lot of extra sweetener is fine too, he said.

Still planning to throw caution to the wind and indulge in a hot-fudge sundae? Then also eat foods rich in omega-3 fatty acids, like salmon, walnuts and flaxseeds, or take a daily DHA capsule. Gomez-Pinilla recommends one gram of DHA per day.

"Our findings suggest that consuming DHA regularly protects the brain against fructose's harmful effects," said Gomez-Pinilla. "It's like saving money in the bank. You want to build a reserve for your brain to tap when it requires extra fuel to fight off future diseases."

The UCLA study was funded by the National Institute of Neurological Disorders and Stroke. Gomez-Pinilla's lab will next examine the role of diet in recovery from brain trauma.

An emerging body of research suggests that Alzheimer's disease may be linked to insulin resistance, constituting a third type of diabetes.  This model is based on several observations including an increased risk of developing Alzheimer's disease for diabetic patients, and reduced insulin levels in the brain tissue of Alzheimer's disease patients. Though intriguing, the existing evidence does not reveal if defective insulin signaling is causative of Alzheimer's or how insulin resistance impacts cognitive function.
Type 2 diabetes is known to increase the risk for Alzheimer's disease. Recent research has found that insulin resistance also develops in the brains of patients with Alzheimer's, which scientists sometimes call "brain diabetes." This brain insulin signaling deficit results in learning and memory disability and could potentially be known as Type 3 Diabetes.
There is much that still remains unknown about the cause of Alzheimer's disease (AD), a form of dementia that affects memory, thinking, and behavior. Two brain changes have long been known to form in the brains of patients with dementia – neurofibrillary tangles and beta-amyloid plaques. Tangles are twisted fibers of tau protein that builds up inside the cells. Plaques are accumulations of protein fragments that build up in the spaces between nerve cells. The two abnormal structures combine to block communication between nerve cells and disrupt the processes needed for them to survive.
But now, a third brain change is emerging as a likely suspect contributing to cognitive deficits in patients with Alzheimer's disease. Brain levels of insulin and insulin receptor (IR) are lower in AD and insulin signaling impairments have been documented in human postmortem analysis and in animal models....
The University of Pennsylvania team examined insulin signaling in human brain tissue postmortem, and concluded that the activation state of many insulin signaling molecules were highly related to memory and cognitive function. They further suggest that insulin resistance is a common and early feature of Alzheimer's disease.
The De Felice group further observed impaired insulin signaling in Alzheimer's brain tissue in rodent and non-human primate model systems as well as from tissue from human patients. They went on to show in a mouse model system of Alzheimer's disease that treatment with a new anti-diabetic drug normalized insulin signaling and remarkably improved cognitive function. Cumulatively, these two new studies strongly support a connection between insulin resistance and Alzheimer's disease and provide hope for new therapeutics in Alzheimer's disease treatment.

Even minuscule amounts of BPA (used in everything from pesticides to water bottles) can scramble hormone signals, and trick fat cells into taking in more fat or mislead the pancreas into secreting excess insulin. Among the most ubiquitous and scrutinized of these...endocrine disruptors is bisphenol, better known as BPA. The chemical is a common ingredient in plastics and food-can linings.
Angel Nadal, a BPA expert at the Miguel Hernandez University in Spain stated that, "When you eat something with BPA, it's like telling your organs that you are eating more than you are really eating"[—]the chemical triggers the release of almost double the insulin actually needed to break down food. High insulin levels can desensitize the body to the hormone over time, which in some people may then lead to weight gain and Type 2 diabetes....
BPA fools a receptor into thinking it is the natural hormone estrogen, an insulin regulator. [Even the tiniest amounts of BPA—a quarter of a billionth of a gram—do] the trick. The effect disappeared when the researchers stripped the specific receptors from the study mice, evidence that they had in fact pinpointed BPA's chemical mechanism, which had previously eluded scientists. In laboratory tests of human cells, the response was even more pronounced....
An estimated 90% of people in developed countries have BPA circulating in their blood at levels often [sic] higher than the threshold for causing hormone disruption used in Nadal's study. This high incidence is due not only to exposures from leaching food packages but also BPA-infused cash register receipts, dental sealants and toilet paper.
Frederick vom Saal, another expert in endocrine disruptors at the University of Missouri-Columbia stated that, "People are seeing effects of BPA down to 1000-fold below [Nadal's threshold]." "It takes so little of this chemical to cause harm."

Participants with diabetes were stratified by insulin therapy at baseline: group A treated with insulin only; group B treated with insulin and oral hypoglycemic agent; and group C receiving no insulin treatment.
During a mean follow-up of 3.9 years, the researchers found that 4.6% of the cohort without diabetes died, compared with 15, 12.5, and 7.3% of groups A, B, and C, respectively. The hazard ratios (HRs) for all-cause mortality were 4.3, 4.2, and 2.0 for groups A, B, and C, compared with individuals without diabetes. The leading cause of death in groups A, B, and C were ESRD, ESRD and CAD, and CAD, respectively. The HRs for these conditions were at least twice as high as the HRs for all-cause mortality, extending to 17.3, 17.9, and 5.1 in groups A, B, and C, respectively, for ESRD.
"Excess mortality persists among people with young-onset diabetes of long duration, with ESRD and CAD as the leading contributors to mortality," the authors write.

[Excuse me? Don't the numbers, if correctly reported, suggest that insulin-and-drug therapy increases mortality by over two-thirds, and insulin-only therapy more than doubles mortality?—DMM]

Children and adolescents participating in moderate to vigorous physical activity have a lower cardiometabolic risk profile. [Physical activity correlated with better waist circumference, blood pressure, triglycerides, HDL cholesterol, and insulin in study subjects] regardless of the amount of time they spend sedentary.
[Based on the findings,] children should be encouraged to increase their participation in physical activity] rather than decrease the amount of time they spend sedentary, "as this appears more important in relation to cardiometabolic health."
[In pooled data from 14 studies (1998-2009) connected to the International Children's Accelerometry Database.] the time spent in moderate to vigorous physical activity has a weak to moderate association with the amount of time children spend sedentary, and this had suggested that both variables might be independently associated with cardiometabolic risk.
[A]ctivities ingrained early in life set the stage for what individuals do in their later and older years. "We're living in an age right now where it's so easy to do no physical activity at all...kids can basically go through an entirely normal childhood existence where, unless they're forced or choose to play sports, they don't have to do anything. This study shows that the more activity that you do, even if it's outside the context of typical exercise, really does make a difference."
In the ICAD analysis, 20,871 children and adolescents from Australia, Brazil, Europe, and the US had [physical-activity levels] monitored for an average of 5.2 days using the accelerometer, and the mean daily time spent engaged in moderate to vigorous physical activity was 30 minutes. The mean daily time spent sedentary was 354 minutes.
Kids in the [most active] tertile spent more than 35 minutes per day engaged in moderate to vigorous physical activity, whereas those in the bottom tertile were moderately or vigorously active just 18 minutes per day. The mean difference in waist circumference between the most active and least active kids with the most sedentary time was 5.6 cm [and 3.6 cm] in those with less sedentary time. Similarly, the difference in systolic blood pressure between the most active and least active kids with the most sedentary time was 0.7 mm Hg[, while there was a 2.6-mm-Hg difference] between the most active and least active kids who reported less sedentary time. The variations in HDL cholesterol, insulin, and triglyceride levels were similar when analyzed by physical-activity levels and sedentary time.
Overall, the results showed that higher levels of physical activity were associated with better cardiometabolic risk factors across the tertiles of sedentary time. In contrast, sedentary time was not associated with any of metabolic outcomes independent of the time engaged in moderate and vigorous activities. The researchers note that they did not qualify what specific activities the children were engaged in while being sedentary. For this reason, reducing television viewing time is still considered an important goal of parents and public-health policy because TV watching is also associated with other unhealthy behaviors, such as snacking and drinking soda.

[Having received an inappropriately substituted prescription in an effort to lower their copay, the patient and his wife] sat for two days at home without insulin administration, choosing not to test his glucose since they knew they didn't have a way to inject the insulin, until the Home Health nurse arrived.
The Home Health nurse reviewed syringe technique with the patient and they ultimately chose to go with the pen. The Home Health nurse expedited the original Rx and reviewed the sliding scale and glucose results from fingersticks. The patient is doing well....
Navigating what doctors prescribe and what insurance companies charge for co-pays can be a major problem. Copays can range from no cost to more than $100, depending on which tier the medication is in....
With the difficulty of navigating...benefits, co-pays and different tiers, following up with patients is imperative. The Home Health nurse visit truly averted disaster.

Federal regulators have warned Johnson & Johnson that it could face fines and other sanctions for selling faulty insulin pumps and delaying disclosures of serious injuries to diabetics who were using its OneTouch Ping and 2020 pumps. The FDA ordered the Animas Corp. unit of J&J to explain why it kept selling pumps known to fail and also to submit a plan to rectify a failure to promptly report cases in which its device might have caused or contributed to death or serious injury....
In the issue with the Animas insulin pumps, some pump keypads for controlling how much insulin is injected were deteriorating prematurely, leading to failures. "We decided to go with a new keypad because it's more durable," [spokesperson Caoline] Pavis said.
But while Animas was lining up the new keypad supplier, it was still selling the older ones. The FDA demanded documents about the company's decision to do that.

A [rancher] was referred to me for assistance in helping with glycemic control....[Over the prior 2-3 years, his injected insulin type had been changed several times in an attempt to improve his fasting blood sugar control. When I saw him, his dose had been increased at each recent doctor visit due to continued high morning blood sugars. He WAS checking blood sugar in the middle of the night and was not having any lows that might trigger a morning spike.]
At our first visit, I asked him to bring his insulin vial/syringes/glucometer, etc. with him on his next visit.
At our second visit, he pulled out a syringe that had been used so many times the numbers were totally worn off! He said he had "gotten good at guessing" when drawing up his dose! I asked him how often he changed syringes. He replied that he had never been told to change syringes—and did not even have a prescription for them—he had been using the present one for over a year and it was from a set of syringes he had used to give his cattle shots!
I gave him a sample of new syringes, made sure he got a prescription, and saved his old syringe as a reminder to myself to never forget to ask the simple questions [about what we assume] people know.

Lesson Learned:
Asking the right questions and having the patient bring their medications and devices and...demonstrate their techniques can prevent future or current problems.

Jeri Mills, MHR, RD/LD, CDE

Five of the seven studies showed a significant inverse association between chocolate consumption and cardiovascular disease. Compared with the lowest levels of chocolate consumption, the highest levels of consumption were associated with a 37% reduction in the risk cardiovascular disease and a 29% reduction in the risk of stroke. There was no association between chocolate consumption and heart failure risk and no association in women between chocolate consumption and the incidence of diabetes.

Lead study author Adriana Buitrago-Lopez, RN, and colleagues noted that “Although overconsumption can have harmful effects, the existing studies generally agree on a potential beneficial association of chocolate consumption with a lower risk of cardiometabolic disorders. Our findings confirm this, and we found that higher levels of chocolate consumption might be associated with a one-third reduction in the risk of developing cardiovascular disease.”

[Six men age 30-65, overweight but otherwise healthy, consumed 2 tablespoons of culinary spices—rosemary, oregano, cinnamon, turmeric, black pepper, cloves, garlic powder and paprika—in each serving of a test meal of chicken curry, Italian herb bread, and a cinnamon biscuit, or an otherwise identical control meal without the spices.]
"We selected [spices that had shown] potent antioxidant activity previously under controlled conditions in the lab."
[The spices increased antioxidant activity in the blood by 13% and decreased insulin response decreased by about 20%.]
Oxidative stress contributes to heart disease, arthritis and diabetes. [The spice dose used provided equivalent antioxidants to those in 5 oz. red wine or 1.4 oz. dark chocolate.]
Adding 2 tablespoons of spices to meals did not cause stomach upset in the participants. "They enjoyed the food and had no gastrointestinal problems...The participants were notified ahead of time that they would be eating highly spiced foods..."

A diet high in saturated fat is a key contributor to Type 2 diabetes...[Type 2 diabetics have overly active immune responses, leaving their bodies rife with inflammatory chemicals. Those who acquire the disease are typically obese and are resistant to insulin....New research adds clarity to the connection:] saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta. <br />
"The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production," says senior study co-author Jenny Y. Ting, PhD... <br />
"Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin resistant. As a result, activation of this pathway by fatty acid can lead to insulin resistance and Type 2 diabetes symptoms."

“[Animals on the high-fat diet were able to handle glucose better. Their glucose tolerance tests improved. Their bodies responded to insulin better. Leucine] improved their ability to metabolize sugar and fats. It markedly improved their pre-diabetic condition. Their metabolic syndrome also improved.” <br />
Mice who were fed a normal diet and given leucine showed no significant effects from [the] supplement. <br />
“[Adding just this one amino acid changed the metabolism in a lot of different pathways. It improved insulin sensitivity, improved ability to metabolize sugar and fats and] overall metabolism improved"....<br />
[Researchers do not propose those with prediabetes or metabolic syndrome add leucine to their diets, but want to perform human trials.] <br />
[Prior in vitro studies found that leucine, 1 of 22 amino acids that serve as building blocks of proteins, affects insulin signaling. Leucine, found in all protein food sources, is often taken in supplements by body builders to increase muscle mass.

[The structured testing group intermittently recorded] blood sugars before and 2 hours after each meal and at bedtime, as well as their meal size and energy levels, over 3 consecutive days. [Every 3 months, they brought the data] to their doctor. [Participating physicians were taught to identify normal patterns and when to make therapeutic interventions—from recommending lifestyle changes to prescribing insulin. The active control group checked] blood sugars as they usually did but did not record them in a systematic way. <br />
At 12 months...the structured group had a significantly greater mean improvement in HbA1c [(-1.2% vs -0.9% control)], lower average preprandial and postprandial glucose [at all meals and bedtime], and significant reductions in mean amplitude of glucose excursions[: mean 4.2 mg/dL]. <br />
[Physicians in the structured study arm] were more likely to recommend a medication change (60% vs 23%), a lifestyle change (41% vs 9%) or both (76% vs 28%)...

[A study—the first—tests the potential connection between autoimmunity and Type 2 diabetes head-on, via components in both humans and mice. R]esearchers fed mice a high-fat diet that would be expected to induce insulin resistance...After 5 weeks, they gave some of the mice [immune suppressant anti-CD20, there was no sign of insulin resistance, and blood glucose levels were normal. All other mice developed insulin resistance. Apparently] in overweight mice—and, most likely, humans—an immune system attack on fat cells...leads to insulin resistance. <br />
Conducting a similar experiment in humans would be much more complicated, both pragmatically and ethically...So to test whether the mice findings might also apply to humans, the researchers took blood samples from 32 obese people, half of whom had insulin resistance. [The researchers found distinct sets of antibodies—proteins created by the immune system to attack specific substances—] in participants with and without insulin resistance.

[Among insulin-resistant subjects, 20 g of apple cider vinegar, 40 g of water, and 1 tsp of saccharine with each meal reduced postprandial (after-meal) glucose 34%.] <br />
Postprandial benefits had been found before. It was thought that vinegar might slow the absorption of carbohydrate into the blood, or slow the breakdown of starches into sugars[, mimicking] the effect of drugs like acarbose... <br />
[In this 2004 ASU study,] vinegar reduced postprandial glucose more in subjects who were highly insulin resistant[, suggesting vinegar increases insulin sensitivity, as does] metformin. <br />
Now studies have found that vinegar at bedtime reduces fasting blood glucose in the morning, indicating that vinegar might promote insulin production, like nateglinide... <br />
[Apple cider vinegar has been touted for centuries for many health benefits, W]ine vinegar, rice vinegar, and white vinegar may be equally good, but] haven’t been studied. Balsamic vinegar apparently is not good; it’s too sugary.

[Comparing the in-vitro levels to normal pancreatic release, researchers found that normal mice released about 2.8 nanograms of insulin per cell, while the cells from “Snapin-on” mice released 7.3 ng—about 3 times normal]....<br />
[Reversing the comparison, normal cells released 5.8 ng of insulin, whereas cells with no Snapin only released 1.1 ng—c. 80% less]. <br />
[On ingestion of glucose, normal] beta cells release an initial burst of insulin almost immediately, then gradually release more [c. 15 minutes later. Type 2 diabetics don’t release this initial spurt when fed glucose, but still have the later gradual] release. <br />
Since the cells with Snapin on made too much insulin, researchers wanted to see if they could use this to restore these mice’s ability to secrete the initial burst of insulin. After [engineering pancreatic beta cells to make the Snapin-on protein, researchers fed glucose to the cells, which] did indeed regain the ability to release that initial insulin burst.

An Italian study of 477 overweight and obese children found wrist circumference accounted for 12% to 17% of differences in insulin resistance, with bigger wrist circumference indicating possible problems. "If our work is confirmed by future studies, wrist circumference could someday be used to predict insulin resistance and cardiovascular disease risk," said Dr. Raffaella Buzzetti, lead author of the study published in the journal Circulation.

Whole almonds (WA), almond butter (AB), defatted almond flour (AF), almond oil (AO) or no almonds [were part of a 75 g available carbohydrate-matched breakfast. Blood glucose, insulin, non-esterified free fatty acids (NEFA), and hunger were tested after breakfast] and a standard lunch.<br />
WA significantly [reduced 2nd-meal and daylong blood glucose] and provided the greatest daylong feeling of fullness. AB and AO decreased [morning blood glucose. Daylong blood glucose was reduced with AO. WA and AO showed greater 2nd-meal insulin response, particularly in the early phase, and also suppressed] 2nd-meal NEFA response....<br />
[Almonds for breakfast decreased blood glucose and increased satiety acutely and after a 2nd meal. Lipids] account for the immediate post-ingestive response, but not for the second-meal response. D]aylong glucose, insulin and NEFA concentrations were attenuated in the WA and AO treatments, indicating an improved hormonal profile[. Effectiveness matched the drug acarbose.]

Fatty liver‚ already associated with insulin resistance‚ may also independently increase the risk for type 2 diabetes... <br />
Individuals with fatty liver tend to have several risk factors for type 2 diabetes[:] excess weight‚ hypertension‚ and metabolic abnormalities....The analysis included more than 11‚000 Koreans who were evaluated for fasting insulin concentration and who received abdominal ultrasound testing‚ then followed up after five years. At baseline‚ 27 percent of subjects had fatty liver and 47 percent of those had baseline insulin concentration in the highest quartile‚ compared to only 17 percent in those without fatty liver. Individuals with fatty liver had significantly more clinical and metabolic abnormalities at baseline‚ such as higher glucose and triglycerides and lower HDL cholesterol. Participants with fatty liver had a significantly higher risk of type 2 diabetes compared to those without fatty liver.

[An experimental‚ ultra–long–acting insulin may be as effective as daily insulin for controlling blood sugar in type 2 diabetics.] <br />
[Degludec is injected] just three times a week. The trial results are published in The Lancet. Results showed that study subjects with type 2 diabetes who took degludec by injection three times a week had similar reductions in hemoglobin A1c as patients who received daily injections of the long–acting insulin glargine (Lantus); however, patients who took degludec had fewer episodes of hypoglycemia. The 16–week study included 245 patients with type 2 diabetes who had high blood sugar in spite of their use of oral drugs to reduce their blood–sugar levels. Patients were randomly assigned to receive metformin and one of three treatment regimens: degludec insulin once a day‚ degludec three times a week‚ or glargine once a day. While blood sugar levels were similar for all treatment groups‚ rates of hypoglycemia were lowest in the once–daily degludec group.

“In the many studies [of] the effect of vitamin D in different cancer types, there is no straight link between use and benefit"... <br />
[Vitamin D may reduce the risk of colon cancer development, with no effect on later stages, and] may increase the risk of prostate, esophagus and pancreatic cancer. [With endometrial cancer,] vitamin D was not beneficial in lean mice, in obese animals it reverses both early and advanced stages...<br />
“[Vitamin D should not be taken lightly. Sufficient amounts have overall health benefits] that have nothing to do with preventing cancer. [Those who want to boost their use of vitamin D must have individual levels tested by a physician"... <br />
A higher dose (25K IU) was used in mice fed the obesity-inducing diet because vitamin D becomes trapped in fatty tissue and thus is reduced in the blood stream...<br />
[Obese mice developed insulin resistance, and vitamin D supplementation reversed it. Vitamin D in lean mice reduced insulin sensitivity in both mouse models.]

Dr. Linden's team identified the primary cellular players in the adenosine-fueled inflammation cascade that contributes to insulin resistance...."Our study clarifies the molecular steps triggered by adenosine, which leads to inflammation linked not only to Type 2 diabetes but to other inflammatory diseases"....Type 2 diabetes is associated with chronic low-grade inflammation. "We believe [insulin resistance involves macrophages, cells] of the body that contribute to inflammation...[Adenosine stimulates macrophages, which release chemicals called cytokines,] molecules that rev up the immune system. We believe it is the cytokines that cause tissues to become less sensitive to insulin." <br />
By using an adenosine receptor blocker, the team prevented the adenosine from activating the macrophages[:] "So the downstream effect of releasing cytokines does not occur"...[T]issues began to better respond to insulin, which reduces blood sugar levels in diabetic animals.

Metabolic syndrome is defined as the presence of any three of the following conditions: <br />
* waist measurement of 40 inches or more for men and 35 inches or more for women<br />
* triglyceride levels of 150 milligrams per deciliter (mg/dL) or above, or taking medication for elevated triglyceride levels<br />
* HDL, or “good,” cholesterol level below 40 mg/dL for men and below 50 mg/dL for women, or taking medication for low HDL levels<br />
* blood pressure levels of 130/85 or above, or taking medication for elevated blood pressure levels<br />
* fasting blood glucose levels of 100 mg/dL or above, or taking medication for elevated blood glucose levels.... <br />
[M]ost people with pre-diabetes develop type 2 diabetes within 10 years, unless they lose 5 to 7 percent of their body weight—about 10 to 15 pounds for someone who weighs 200 pounds—by making changes in their diet and level of physical activity. People with pre-diabetes also are at increased risk of developing cardiovascular disease.

“Glutamate, a major signaling molecule in the brain and pancreas, is secreted together with glucagon by alpha cells and affects beta cell integrity...[An imbalance toward more alpha cells and fewer beta cells, as in Type 1 and Type 2 diabetes,] could result in further beta cell destruction.”
Glutamate toxicity is a new mechanism of beta cell destruction not previously known...[Alpha cells were not previously suspected as] a cause of beta cell damage... <br />
The study also found a [protective effect from a protein. GLT1. that controls glutamate levels outside the beta cells, "]like a thermostat controlling the microenvironment of beta cells with respect to glutamate concentration".... <br />
Glutamate poisoning is a new candidate mechanism for beta cell destruction[, joining] high glucose, buildup of a protein called amyloid, and free fatty acids, which are found in patients with type 2 diabetes.

[Better BMI, waist size, and insulin sensitivity were] independent of daily calorie intake, and instead appeared to be associated with changes in adiposity (fat levels) related to the increased walking... <br />
Previous studies have shown that exercise interventions can reduce insulin resistance, this is the first study to show that real-life attempts to increase physical activity can be effective at improving insulin sensitivity. <br />
The researchers suggested that a relatively inactive person who changed their behavior over the course of five years to reach the widely recommend goal of 10,000 steps per day would improve his insulin sensitivity threefold compared to someone who increased his walking to 3,000 steps five days a week. They concluded that “These findings, confirming an independent beneficial role of higher daily step count on body-mass index, waist-to-hip ratio, and insulin sensitivity, provide further support to promote higher physical activity levels among middle-aged adults.”

[To 18 non-insulin-dependent diabetic patients, p]syllium fiber or placebo was administered twice during each 15-h crossover phase, immediately before breakfast and dinner. No psyllium fiber or placebo was given at lunch, which allowed measurement of residual or second-meal effects. For meals eaten immediately after psyllium ingestion, maximum postprandial glucose elevation was reduced by 14% at breakfast and 20% at dinner relative to placebo. Postprandial serum insulin concentrations measured after breakfast were reduced by 12% relative to placebo. Second-meal effects after lunch showed a 31% reduction in postprandial glucose elevation relative to placebo. No significant differences in effects were noted between patients whose diabetes was controlled by diet alone and those [who took oral hypoglycemics. P]syllium as a meal supplement reduces proximate and second-meal postprandial glucose and insulin concentrations in non-insulin-dependent diabetics.

“Insulin has this fundamentally important ability of suppressing lipolysis, [during which triglycerides in fat are broken down and fatty acids are released. Finding] this is mediated in a large part by the brain is surprising...The major lipolysis-inducing pathway in our bodies is the sympathetic nervous system and here the studies showed that brain insulin reduces sympathetic nervous system activity in fat tissue. In patients who are obese or have diabetes, insulin fails to inhibit lipolysis and fatty acid levels [rise]. The low-grade inflammation throughout the body...commonly present in these conditions is believed to be mainly a consequence of these increased fatty acid levels...When brain insulin function is impaired, the release of fatty acids is increased. This induces inflammation, which can further worsen insulin resistance, the core defect in type 2 diabetes. [I]mpaired brain insulin signaling can start a vicious cycle since inflammation can impair brain insulin signaling.”

The study involved 135 people with an average age of 67 from Hisayama, Japan. The participants had several diabetes glucose tests to measure blood sugar levels. They were also monitored for symptoms of Alzheimer's disease over the next 10 to 15 years. During that time, about 16 percent developed Alzheimer's disease. <br />
After the participants died, researchers examined their autopsied brains for the physical signs of Alzheimer's disease, called plaques and tangles. While 16 percent had symptoms of Alzheimer's disease while alive, a total of 65 percent had plaques. <br />
The study found that people who had abnormal results on three tests of blood sugar control had an increased risk of developing plaques. Plaques were found in 72 percent of people with insulin resistance and 62 percent of people with no indication of insulin resistance. However, the study did not find a link between diabetes factors and tangles in the brain.

"In Type 1 diabetes, your pancreas isn't making insulin. In Type 2 diabetes, your tissues are insensitive to insulin because of problems in the insulin receptor. Type 3 is where that insulin receptor problem is localized in the brain....[Some older] individuals start to have less effective insulin signaling, including in the brain"[, making the brain more vulnerable to large sticky plaques of amyloid beta protein,] a hallmark of Alzheimer's...<br />
[Short strands of the protein, known as] ADDLs, attack memory-forming brain cells...[In lab tests, insulin blocked the effects of ADDLs in rat nerve cells, an effect amplified by a drug that] increases insulin sensitivity. <br />
Several studies have found that diabetics have a higher risk of getting Alzheimer's... <br />
[Earlier research reports] diabetics who take insulin plus a range of anti-diabetic medications, including an older pill known as a sulfonylurea], have a lower risk of developing Alzheimer's than diabetics who only take insulin.

[Relationships seen in adolescents between insulin sensitivity and fatty liver, belly fat, and total body fat, along with additional potential early markers of insulin resistance and metabolic syndrome, have been found] in healthy 7-9 year-old children, including fat in muscle cells, blood pressure, physical activity, and birth weight....
The study of more than 100 healthy children, ages 7-9, found that fat in the liver, abdominal fat, and fat oxidation predicted insulin resistance and appear to be early markers for the metabolic syndrome via a mechanism of impaired lipid metabolism and fat oxidation. Impaired metabolic function may be due, in part, to pre-and post natal factors that are modified by current physical activity. Therefore, race, low or high pregnancy weight and/or birth weight, and low physical activity collectively create a phenotype for poor metabolic function leading to increased risk for insulin resistance in young children.

A good portion of the book is dedicated to the discussion of exercise, especially in comparison to the brief recommendations typically given, but don't let the title fool you, the book is very comprehensive.
Most impressive about the book, is the way that Bedingfield uses analogies to explain the complexities of diabetes and its treatment. He has taken the complex explanations and medical terminology out, and replaced them with descriptions of everyday objects and processes that are understandable to the masses. For example, when explaining insulin resistance Bedingfield describes the "doors" to the muscle and fat cells as having "rusty hinges" and thus requiring more insulin to open them. He goes on to say that "exercise has the same effect as if you were to take sandpaper and WD-40 to the rusty hinges." The entire book is in this style, with simple explanations and cartoonish drawings to make simple a disease that many patients struggle to understand.

[New research has] analyzed the reputed health benefits of cashew tree products on diabetes, notably whether cashew extracts could improve the body's response to its own insulin....
"Of all the extracts tested, only cashew seed extract significantly stimulated blood sugar absorption by muscle cells," says senior author Pierre S. Haddad, a pharmacology professor at the University of Montreal's Faculty of Medicine....
Cashew tree products have long been alleged to be effective anti-inflammatory agents, counter high blood sugar and prevent insulin resistance among diabetics. "Our study validates the traditional use of cashew tree products in diabetes and points to some of its natural components that can serve to create new oral therapies," adds Dr. Haddad, who is also director of the Canadian Institutes of Health Research Team in Aboriginal Anti-Diabetic Medicines at the University of Montreal.

"Current drug development efforts target immune cells (macrophages, T-cells) to eliminate this hyperinflammation. Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target adipocytes (fat cells)," explains Moscat, principal investigator of the study...
In normal cells, explains Moscat, PKC-zeta regulates the balance between cellular inflammatory responses to maintain glucose control. During obesity-induced inflammation, however, the function of PKC-zeta changes and the molecule begins to promote inflammation by causing adipocytes to secrete a substance (IL-6) that travels in large quantities to the liver to cause insulin resistance.
"We believe a similar mechanism of action is at play in malignant tumor development. Now we are trying to understand how PKC-zeta regulates IL6 to better determine how we can manipulate the protein to help prevent diabetes and cancer," he adds.

A nutritional supplement containing 40 milligrams of resveratrol was [given daily to 10 randomized subjects (10 others got a placebo)] for six weeks....
[The resveratrol compound suppressed] generation of free radicals, or reactive oxygen species, unstable molecules known to cause oxidative stress and release proinflammatory factors into the blood stream, [damaging] the blood vessel lining.
[It also apparently suppressed] the inflammatory protein tumor necrosis factor (TNF) and other similar compounds that increase inflammation in blood vessels and interfere with insulin...causing insulin resistance...
These inflammatory factors...have an impact on the development of type 2 diabetes, aging, heart disease and stroke...
Blood samples from the [placebo group] showed no change in these pro-inflammatory markers.
The study didn't eliminate the possibility that something in the extract other than resveratrol was responsible for the anti-inflammatory effects.

Researchers reported at EASD that metformin appears to have specific effects on endothelial function, which might help explain why metformin treatment is associated with decreased risk of cardiovascular disease in Type 2 diabetes....Metformin treatment versus placebo was associated with a decrease in vWf of 11% (P < .001); a decrease in sVCAM-1 of 5% (P < .001); a decrease in t-PA of 15% (P < .001); a decrease in PAI-1 of 21% (P = .001); and a decrease in the endothelial dysfunction standard deviation score of 7% (P < .001). Changes in urinary albumin excretion and sE-selectin were not significant. Metformin treatment versus placebo was associated with a decrease in CRP of 17% (P = .036); a decrease in sICAM-1 of -5% (P = .004); and a decrease in the inflammation standard deviation score of -5% (P = .074). "Improvements in endothelial function explained about 35% of the reduced risk of macrovascular morbidity and mortality associated with the use of metformin," said Dr. Kooy.

[Prior research indicates] that certain "fat genes" [correlate] with excessive fat storage in cells[. Yet a study culture of cells in all of which] fat genes were expressed, or activated...varied drastically—from nearly zero in some [cells] to pervasive in others—in how much fat they stored...."[N]ot all biological information in cells is encoded in the genetic blueprint…. [V]ariability in fat storage is dependent on how...cells process insulin, [which triggers] the uptake of glucose from the blood into...liver, muscle or fat cells"....[D]ifferences in fat storage depend not on fat-gene expression but on variations in a cascade of events within an "insulin-signaling pathway"..."[A] small variation at the beginning of the cascade can lead to a drastic variation [at the end]"..."[S]ingle cell profiling" using [various] imaging techniques...precisely compare[d] fat storage in cloned cells having the same fat genes expressed[, allowing comparison of] the inner workings of individual cells.

In 2005, the average American consumed 64kg of added sugar, a sizeable proportion of which came through drinking soft drinks. [New evidence suggests that] consumption of fructose-sweetened but not glucose-sweetened beverages can adversely affect both sensitivity to the hormone insulin and how the body handles fats, creating medical conditions that increase susceptibility to heart attack and stroke. In the study, overweight and obese individuals consumed glucose- or fructose-sweetened beverages that provided 25% of their energy requirements for 10 weeks. During this period, individuals in both groups put on about the same amount of weight, but only those consuming fructose-sweetened beverages exhibited an increase in intra-abdominal fat. Further, only these individuals became less sensitive to the hormone insulin (which controls glucose levels in the blood) and showed signs of dyslipidemia (increased levels of fat-soluble molecules known as lipids in the blood).

A gene known as proliferator-activated receptor coactivator 1 (PGC-1 ), a key regulator of glucose content...is also decreased in Alzheimer' disease dementia cases[, decreases] with progression of the...disease, and positively correlates with brain accumulation of β-amyloid, an abnormal protein highly linked to Alzheimer's disease dementia and brain degeneration. This evidence...suggests, for the first time, a strong relationship between decreased content of a gene responsible for Type 2 diabetes in Alzheimer's disease dementia cases..."[F]urther mechanistic studies in our laboratory [provide evidence] that promoting PGC-1 content in brain cells, using a transgenic mouse model of Alzheimer's disease, attenuates hyperglycemic-mediated production of β-amyloid...These findings...for the first time tentatively link Type 2 diabetic metabolic defects to increasing dementia mediated by β-amyloid production."

'55% of all participants--even those in the control group who received no health-related intervention--reduced...sugar consumption by 47 [g daily, accounting] for an average 33% decrease in insulin secretion....59% of all participants increased their fiber consumption by an average of 5 g per day, resulting in an average of 10% less visceral fat...[T]eenagers in the control group might have changed their diets because they knew the purpose of the study and were more motivated to make changes. [B]ecause the control group members also changed their diets, "intensive interventions may not be necessary to achieve modification in sugar and fiber intake." Individuals who reduced added sugar intake by the equivalent of 1 can of soda per day or increased fiber intake by the equivalent of a cup of beans showed improvements in key risk factors for Type 2 diabetes, specifically in insulin secretion and visceral fat. Improvements...were equally likely to occur in control group participants.'

Not all [type 2 diabetics develop] Alzheimer's disease, and...not all Alzheimer's...cases are diabetic. However, [recent] epidemiological [analysis] indicates that, relative to healthy elderly subjects, [same-age type 2 diabetics] are twice as likely to develop Alzheimer's...dementia. The reason is not known....[A] gene known as proliferator-activated receptor coactivator 1 - (PGC-1 ), a key regulator of glucose content currently investigated as a potential therapeutic target for type-2 diabetes, is also decreased in Alzheimer'[s] cases...PGC-1 decreased in Alzheimer' disease dementia cases with progression of the clinical disease and positively correlates with brain accumulation of β-amyloid, an abnormal protein highly linked to Alzheimer'[s] dementia and brain degeneration. This evidence is of high interest to the field and suggests, for the first time, a strong relationship between decreased content of a gene responsible for type-2 diabetes in Alzheimer's...cases.

In a UM clinical trial recently published in the online journal Cell Transplantation, 25 patients achieved better insulin production, lower blood-sugar levels and reduced need for insulin injections.

In the trial, still in its pilot stage, doctors extracted immature adult stem cells from the patients' own bone marrow, purified and concentrated them, and injected them into arteries near the pancreas. They then put the patients into hyperbaric oxygen chambers like those used for divers with decompression sickness -- also called the ''bends'' -- and subjected them to 10 hours of pure oxygen at 2.4 times the atmospheric pressure at ground level.

Researchers believe the high-pressure oxygen pulled extra stem cells from the patients' bone marrow, adding to the stem cells injected near the pancreas. They say the immature stem cells developed into pancreatic cells, regenerating the pancreas' ability to produce natural insulin.

"While vascular risk factors have been studied as predictors of AD, few studies have assessed their influence on disease progression"...To investigate, [researchers] examined prediagnosis vascular risk in 156 patients with incident AD followed for a mean of 3.5 years. The main outcome measure was the change in a composite score of cognitive ability from diagnosis onward.

A generalized estimating equation model showed an overall decline in composite cognitive score of 0.08 SD per year (p < 0.001).

In models adjusting for age, race/ethnicity, and years of education, associations were observed between higher cholesterol (total and LDL cholesterol) concentrations, a history of diabetes, and faster cognitive decline.

Specifically, each 10-mg/dL increase in total cholesterol or LDL-C concentration was associated with an additional 0.10-SD decrease in cognitive score per year. Diabetes was associated with an additional 0.05-SD decrease in cognitive score per year of follow-up.

'Diabetes is associated with increased risk for Alzheimer's disease (AD), but a new study of metformin suggests that diabetes treatments might bear some of the blame...[M]etformin increased insulin's reduction of intracellular and extracellular beta-amyloid accumulation, but metformin by itself actually increased levels of the Alzheimer's-linked peptides...[Obervation] in vitro and in animal models of AD raises the specter of a wave of new Alzheimer's cases in diabetic patients who have been taking metformin for years. It is the most popular antidiabetic drug in the United States and one of only two oral antidiabetics on the World Health Organization List of Essential Medicines (along with glibenclamide). In 2006, there were 35 million prescriptions for generic metformin filled in the United States...[A]lthough this was an animal study, the findings are worrisome enough that physicians should promptly follow up any complaints of cognitive decline in patients taking metformin.'

Within a week after the gene was delivered using a disarmed virus...blood sugar [of Type 1 diabetic mice] returned to normal and remained that way for the rest of their lives...[N]eurogenin3 goes into the mature liver cells and causes them to make small quantities of insulin, enough to reduce blood sugar levels to normal[, an effect that lasts] about 6 weeks...[Permanent insulin-producing cells appear] later, clustered around the portal veins...that carry blood from the intestines and abdominal organs to the liver[, forming] from a small population of adult stem cells usually found near the portal vein. [These stem cells] serve as a safety net[;] in case of liver injury[, they] activate to form mature liver...or bile duct cells.
[Neurogenin3 directs them to become] insulin-producing islet cells located in the liver. The mature liver cell cannot make this change [permanently].
The islet cells in the liver look similar to those made by pancreas after an injury...

Coffee [seems to inhibit] developing Type 2 diabetes (Nutrition Reviews, 2007-04)....Coffee [correlates with] reduced risk of several cancers[:] mouth, throat[,] esophagus (American Journal of Epidemiology, 2008-12)[,] colon, liver and endometrium (Internationall Journal of Cancer, 2009-04). Women who drink at least 4 cups of coffee a day [seem] somewhat less likely to suffer a stroke...(Circulation online, 2009-02)....[Finns] who drank 3 to 5 cups of coffee daily were 65% less likely to [develop] Alzheimer's...(Journal of Alzheimer's Disease, 2009-01).
[D]ark chocolate can relax blood vessels, making them more flexible (American Journal of Clinical Nutrition, 2008-12)[; help] blood vessels dilate and [lower] blood pressure in overweight people [(AJCN 2008-07);] improve insulin sensitivity as well as blood pressure (Journal of Nutrition, 2008-09)[; lower] platelet reactivity, [improve] cholesterol profiles and [decrease] inflammatory markers...(Southern Medical Journal, 2008-12).

[The] ;Memory in Diabetes (MIND) study, a sub-study of the Action to Control Cardiovascular Risk in Diabetes Trial (ACCORD), found a statistically significant inverse relationship between A1C levels...and subjects' scores on four cognitive tests....psychomotor speed, global cognitive function, memory and multiple task management.
"One of the little known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's dementia...This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss"....Previous studies have shown that [diabetics] are 1.5 times more likely to experience cognitive decline and develop dementia...The ACCORD-MIND study supports the idea that the brain's chronic exposure to elevated blood glucose levels may be part of the explanation for this phenomenon.

A few minutes of intense exercise a week is [at least] as good as a half-hour of moderate physical activity a day for reducing...risk of developing type 2 diabetes....[A]erobic exercise programs can boost sensitivity to...insulin. The high-intensity program...also directly reduced...blood sugar levels--something that standard exercise programs have not been shown to do....
[Researcher Timmons suggested] four to six 30-second bouts of intense exercise, such as cycling or running up stairs, twice a week [as] appropriate for people 20 to 40 years old who are in good health but not fit...[P]eople with diabetes or heart disease should gradually increase their activity under a doctor's supervision.
Recommendations for high intensity, short duration exercise could one day replace current physical activity guidelines, Timmons said. "Only large scale trials could prove this," he said. "But there is mounting evidence that doing this new protocol will deliver the same reductions in risk factors."

[I]nsulin resistance [is implicated] in sodium retention and expansion of extracellular fluid volume[, so] insulin-resistant individuals might have increased blood pressure sensitivity to dietary salt...
[I]nsulin resistance is considered the underlying mechanism of metabolic syndrome...[Researchers proposed that those] with the syndrome would likely be sensitive to a dietary salt intervention....[and] found a graded association between an individual's number of risk factors for metabolic syndrome and blood pressure response during...dietary trials. [In a] low-sodium intervention...[those] with no risk factors had a mean blood pressure decline of 4.3/1.86 mm Hg versus a 9.39/6.06 mm Hg decline for people with 5 risk factors...[T]he findings...have several implications for health policy [according to an accompanying commentary, including t]he value of lifestyle interventions in people with metabolic syndrome [and its potential value among those at risk.]

As I learned at a seminar at the University of California San Francisco last week, much of the genetic programming comes from stress. Stress experienced in the womb, or as an infant seems particularly likely to encourage fatness. But if your mother, or her mother, or even her mother's mother was stressed, weight-gaining tendencies may be passed down to you.

(It's not that your genes change in response to stress. They don't. But they can get turned on or off, or their functions can be modified by the environment, or your ancestors' environment. This is called "epigenetics" or, more broadly, "environmental determinants.")

If you have this early programming, stress will continue to promote weight gain throughout your life. This doesn't mean you can't get in shape. You can! But buying into the "blame the patient" idea will make things harder. It will increase your stress and lower your self-confidence.

"You can make just as big as an effect doing this as you can by doing hours and hours of endurance training each week."....[J]ust seven minutes of exercise each week helped a group of 16 men in their early twenties control their insulin. The volunteers,...relatively out of shape but otherwise healthy, rode an exercise bike four times daily in 30 second spurts two days a week. After two weeks, the young men had a 23% improvement in how effectively their body used insulin to clear glucose, or blood sugar, from the blood stream...The effect appears to last up to 10 days after the last round of exercise..."[I]f you are doing tense muscle contractions during sprints or exercise on a bike you really enhance insulin's ability to clear glucose out of the bloodstream," Timmons said. "If you go for a jog or a run you oxidise glycogen but you are not depleting the glycogen in your muscles. The only way to get to this glycogen is through very intense contractions of the muscles."

Beta cell failure in the pancreas leads to both type 1 and 2 diabetes. Especially in people with Type 1...[beta] cells are killed by high concentrations of inflammatory signals, but scientists have been at a loss to explain [their demise] in people with [type 2]....[Investigators studying] cell samples taken from people with and without type 2 diabetes...found more than 30 times the amount of an inflammatory factor called CXCL10 in [diabetics]...[H]uman pancreatic cells [exposed] to CXCL10 in the laboratory [lost] beta cells...[T]he ability of the [remaining] cells to make and secrete insulin declined.
The researchers [believe they can use] a key protein in the immune system pathway CXCL10 uses to achieve [its pancreatic effects], called TLR4, to find a way to stop the process[:] "[U]sing anti-inflammatory targets of the TLR4 signaling pathway will be of high importance to rescue the beta cell from inflammation-induced self-destruction and [to] preserve beta cell function and mass."

Maedler's team suspected that inflammatory factors might play a key role there as well. Indeed, inflammatory markers are found in obesity, insulin resistance and diabetes, they explained. Earlier studies also showed that low-grade inflammation and activation of the innate immune system—the body's first line of defense--can lead to beta cell failure in type II diabetes.
They've now found that the inflammatory factor CXCL10 (also known as Interferon-gamma-inducible Protein-10, or IP-10) is an important trigger for β cells' destruction. They found that hormone-producing cells isolated from patients with type 2 diabetes secrete CXCL10 and contain more than 30 times the amount of the CXCL10 message in the form of RNA than do cells from patients without diabetes.
The new data suggest a potential mechanism for the switch from β cells' proliferation to their programmed cell death...

[The] obese have an increased risk of developing type 2 diabetes, in part because they often become resistant to...insulin. Resistin is a soluble factor produced by fat cells (adipocytes) that is linked to the development of insulin resistance in mice. However, studies have thus far failed to determine such a clear association in humans. But now, Mitchell Lazar and colleagues, at the University of Pennsylvania, Philadelphia, have determined that human resistin contributes to the development of insulin resistance in mice...[R]esistin is produced mainly by immune cells known as macrophages in humans, whereas it is produced by adipocytes in mice...[Mice engineered to produce resistin only in the human manner] were fed a high-fat diet[;] they developed inflammation of the fat tissue, which led to altered levels of fats in the blood and, ultimately, to insulin resistance. [F]uture studies using these mice [may] help determine the therapeutic potential of modulating levels of human resistin.

Diabetics have a significantly greater risk of [Alzheimer's disease] and other dementia, [according to] data from an ongoing study of twins. The risk of dementia is especially strong if the onset of diabetes occurs in middle age...[G]etting diabetes before the age of 65 corresponds to a 125% increased risk for Alzheimer's disease....[T]he chances of a diabetic developing Alzheimer's disease may be even greater in real life than in the study[: the researchers list] factors that might have led them to underestimate the risk of dementia...among those who develop diabetes before the age of 65. Diabetes usually appears at a younger age than dementia...Diabetes [yields] a higher mortality rate, which may reduce the size of the sample of older adults...[Some 30% of older diabetics] have not been diagnosed. The [study implicates] adult choices such as exercise, diet and smoking, as well as glycemic control in patients with diabetes, in affecting risk for Alzheimer's disease and diabetes...

Researchers found that exposure to air pollution, over a period of 24 weeks, exaggerates insulin resistance and fat inflammation. “[O]besity has reached epidemic proportions with 34% of adults in the US, ages 20 and over, meeting the criteria...Obesity and diabetes are very prevalent in urban areas and there have been no studies evaluating the impact of poor air quality on these related conditions until now.”
Type 2 diabetes, a consequence of obesity, has soared worldwide with a projected 221 million people expected to suffer from this disease in 2010, a 46 percent increase compared to 1995...[S]cientists fed male mice a diet high in fat over a 10-week period to induce obesity and then exposed them to either filtered air or air with particulate matter for six hours a day, five days a week, over a 24-week period...The air pollution level inside the chamber containing particulate matter was comparable to levels a commuter may be exposed to in...many metropolitan areas in the U.S.

[Study of] sleep-disordered breathing (SDB) and insulin resistance... definitively link[s] SDB to pre-diabetic changes in insulin production and glucose metabolism...[Previous studies used surrogates to measure body fat and to assess the body's response to insulin,] without investigating the interaction...between reduced insulin sensitivity and increased insulin production...Dr. Punjabi...used [DEXA], a highly precise technique for assessing body fat, and frequently sampled intravenous glucose tolerance test (FSIVGTT)...a detailed picture of the subject's insulin sensitivity over time....Each subject underwent a sleep study [and an FSIVGGT] the following day.
"...SDB was strongly associated with a decrease in the three major metabolic pathways that the body uses to metabolize glucose--insulin sensitivity, glucose effectiveness, and pancreatic cell function--independent of adiposity...multiple physiological deficits that increase the predisposition for type 2 diabetes mellitus."

The researchers examined the association between the individual components of metabolic syndrome (hypertension, large waist circumference, high triglycerides, low HDL cholesterol, and elevated fasting glycemia) and the risk of incident dementia and its subtypes (Alzheimer's disease and vascular dementia)....15.8% of the participants had the metabolic syndrome, which increased the risk of incident vascular dementia, but not Alzheimer's disease, independent of sociodemographic characteristics...[T]he only component of the metabolic syndrome that was significantly associated with the incidence of all-cause [and vascular] dementia was high triglyceride levels....A significant association was also observed between diabetes and all-cause [and vascular] dementia....[Lead author Dr. Christelle Raffaitin commented:] "Our next step is to study the associations between cognitive decline -- the stage before dementia -- and metabolic syndrome and its components."
Diabetes Care Jan. 2009;32:169-174.

'Extremely low volume high-intensity interval training (HIT) has recently been shown to cause...improvements to aerobic performance...Sixteen young men...performed 2 weeks of supervised HIT...a total of 15 min of exercise (6 sessions; 4-6 x 30-s cycle sprints per session)....Following 2 weeks of HIT, the area under the plasma glucose, insulin and NEFA [free or nonester fatty acids] concentration-time curves were all reduced (12%, 37%, 26% respectively...). Fasting plasma insulin and glucose concentrations remained unchanged, but there was a trend towards reduced fasting plasma NEFA concentrations post-training (pre: 350 +/- 36 v post: 290 +/- 39 mumol * l-1, P=0.058). Insulin sensitivity as measured by the Cederholm index was improved by 22.5%...Aerobic cycling performance was improved by ~6% (P<0.01)...The efficacy of a high intensity exercise protocol, involving only ~250 kcal work each week, to substantially improve insulin action in young sedentary subjects is remarkable.'

Male mice were divided into...high-fat (HF), HF+[pomegranate]seed oil (HF+POMo) or lean control (LN). In the HF and HF+POMo groups, mice [had unlimited access to] high-fat chow (60% energy from fat). Mice in the HF+POMo group were supplemented with 62 mg of POMo/d. The LN group consumed [restricted 10%] fat) chow to maintain body weight...
Weight gain was associated with an increase in biomarkers of cholesterol profile, glucose sensitivity, adipose tissue accumulation and systemic low-grade inflammation (P<0.05).
POMo only altered body weight accumulation, final body weight, leptin, adiponectin and insulin (P<0.05). Researchers found despite a similar level of energy intake, HF mice had a greater concentration of leptin and a lower concentration of adiponectin compared to HF+POMo mice.
POMo intake was associated with an improvement in insulin sensitivity, suggesting the risk of developing type 2 diabetes may have been reduced; however, cardiovascular disease risk did not change.

Children with diabetes are at an increased risk for developing eating disorders and researchers want to know if it's their disease or treatment that's to blame. "Diabetes treatment prescribes obsessive food behavior, such as carbohydrate restriction," said Dr. Deborah Young-Hyman..."We want to know if those prescribed behaviors contribute to disordered eating and/or whether there are physiological mechanisms which prevent children with diabetes from controlling their eating behavior. For example, treatment with insulin makes you hungry and can cause you to gain weight....If we don't approach weight control as dieting, place less emphasis on food restriction and focus on healthy nutrition and usual eating patterns, we can help patients gain more control over their eating behaviors and their treatment without adoption of maladaptive weight management strategies...[F]eeling in control of your illness is one of the keys to successful treatment and good psychological adjustment."

Many health-care providers are unaware of the association between snoring, sleep apnea, and diabetes, and [miss] treatment opportunities..Everyone with diabetes should be screened routinely for the symptoms of snoring and sleep apnea. When people with diabetes and their sleep partners are asked the following three questions, nearly half will respond positively and can be expected to benefit from a referral to a sleep specialist: Do you snore? (While not everyone who snores has sleep apnea, just about everyone with sleep apnea snores.) Do you wake up tired after a full night’s sleep? Do you have high blood pressure? If you answered yes to any of these questions but your health-care provider has not talked about sleep apnea with you, bring it up at your next appointment. Treating sleep apnea can have remarkable benefits: Not only will you sleep better, but your level of insulin resistance may decrease significantly and you may reduce your risk of cardiovascular disease.

"Men who received vitamin K supplementation had less progression in their insulin resistance...," said Sarah Booth, senior author..."Conversely, we saw progression in insulin resistance in women who received vitamin K supplementation, and in the men or women who were not given vitamin K..." [B]oth men and women took...500 micrograms of vitamin K [daily], five times the [recommended] Adequate Intake (AI)...In addition to improved insulin resistance, the supplemented men had lower blood insulin levels....The authors speculate that weight might explain why only...men improved their insulin resistance. "[We had more] obese or overweight women in the vitamin K supplementation group compared to the male[s]...If there is excess fat, vitamin K [is stored in it and] may not be [available] to process glucose."...[T]he study dosage is attainable by [a diet including such] good sources of vitamin K [as] brussels sprouts, broccoli, and dark, leafy greens, such as spinach and collards.

New research from the University of Cincinnati (UC) implicates the primary chemical used to produce hard plastics—bisphenol A (BPA)—as a risk factor for the metabolic syndrome and its consequences.

In a laboratory study, using fresh human fat tissues, the UC team found that BPA suppresses a key hormone, adiponectin, which is responsible for regulating insulin sensitivity in the body and puts people at a substantially higher risk for metabolic syndrome.

Metabolic syndrome is a combination of risk factors that include lower responsiveness to insulin and higher blood levels of sugar and lipids. According to the American Heart Association, about 25 percent of Americans have metabolic syndrome. Left untreated, the disorder can lead to life-threatening health problems such as coronary artery disease, stroke and type 2 diabetes.

[O]besity and Type 2 Diabetes Mellitus (T2DM) can contribute to mild neurodegeneration with features common with Alzheimer's disease (AD) - the first study to show that obesity can cause neurodegeneration...appeared in the Journal of Alzheimer's Disease Volume 15:1 (September 2008). [L]ead researcher Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, utilized chronic high fat diets to cause a two-fold increase in mean body weight [in] animal models, [in which] there was a marginally reduced mean brain weight and a significantly reduced mean brain weight/body weight ratio, providing evidence that obesity with T2DM is sufficient to cause mild global atrophy in the brain. De la Monte says, "In essence, the brain shrinks and several biochemical and molecular abnormalities found in patients with AD, including brain insulin resistance, develop with chronic obesity and T2DM. However, the extent of the abnormalities in no way matches AD."

Obesity [is] associated with an abnormal fat metabolism in the muscle. [A]ccumulated fat by-products inside the muscle affect insulin resistance. To avoid the build up of fat by-products, fat must either be oxidized (burned, as in exercise) or stored (as benign fat) in muscle....In one session [five obese] women overate and did not exercise; in a follow-on session they overate and did exercise. The researchers found that:
* the body's fat-burning oxidation rate was reduced after one day of overeating;
* conversely, just one session of exercise increased the rate of fat-burning oxidation; and
* exercise increased the amount of fat that would eventually be stored in the muscle.
The findings indicate that even one bout of exercise helps to reduce the fat by-products inside the muscle, which affects the insulin sensitivity[, and] that a single session of exercise "steers" muscle fat towards oxidation, thereby avoiding the accumulation of fat by-products.

A recent study randomized a group of men and women to consume either a diet high in beta-glucan (a type of fiber) from oats or a diet...not containing the compound. Those consuming the beta-glucan experienced positive effects on insulin response; the subjects who were obese had a significant reduction in blood pressure, too...Oatmeal tip: You may have heard that the old-fashioned, slow cooking oats are a better health choice than instant oatmeal...Instant oatmeal has a significantly higher glycemic impact. So, buy the old-fashioned oats (steel cut are the best) and do this if you’re in a hurry: Pour half a cup of the oats in a microwave-safe bowl and add just enough water to cover every bit of the oats. Microwave on high for 30 to 45 seconds. Stir, and see if the consistency is to your liking. [Or, pour boiling water to cover dry oats in a bowl, let steep a few minutes, then stir.] You may want to add a bit of milk[, cream, or butter.]

[M]uscles account for only about 40% of your body weight, [but] can take up 80% of any glucose load [from] carbohydrate intake...[B]y enhancing your muscles’ capacity to take up glucose with or without insulin, exercise comes closer than anything else to “erasing” your mistakes with your food, insulin, or other medications that lead to hyperglycemia...{P]eople can eat more carbohydrate and process it more effectively following hard or prolonged workouts....When your insulin works better, you need less of it to have the same or even a greater glucose-lowering effect. The greatest enhancement in insulin action occurs in the few hours following exercise when your muscle glycogen is most depleted and requires replenishment. During this time, you will likely need considerably less insulin to process any carbohydrates that you eat, and you can get away with eating more carbs after exercise, particularly if it was strenuous and prolonged.

'The potential role of arsenic in diabetes development is supported by experimental and mechanistic evidence'...Insulin-sensitive cells that are exposed to insulin and sodium arsenite appear to take in less glucose than cells exposed only to insulin. Arsenic could also influence genetic factors that interfere with insulin sensitivity and other processes, or could contribute to oxygen-related cell damage, inflammation and cell death...'From a public health perspective, confirmation of a role for arsenic in diabetes development would add to the concerns posed by the carcinogenic, cardiovascular, developmental and reproductive effects of inorganic arsenic in drinking water....Given widespread exposure to inorganic arsenic from drinking water worldwide, elucidating the contribution of arsenic to the diabetes epidemic is a public health research priority with potential implications for the prevention and control of diabetes.'

Turmeric-fed obese mice showed significantly reduced inflammation in fat tissue and liver compared to controls. They speculate that curcumin, the anti-inflammatory, anti-oxidant ingredient in turmeric, lessens insulin resistance and prevents Type 2 diabetes in these mouse models by dampening the inflammatory response provoked by obesity....
Turmeric (Curcuma longa) has no known dose-limiting toxicities in doses of up to at least 12 grams daily in humans. The researchers tested high doses of a dietary curcumin in two distinct mouse models of obesity and Type 2 diabetes: high-fat-diet-fed male mice and leptin-deficient obese female mice, with lean wild-type mice that were fed low-fat diets used as controls....
[Curcumin from turmeric was also associated with a small but significant decline in body weight and fat content in the mice], despite level or higher calorie consumption, suggesting that curcumin beneficially influences body composition....
For now, the conclusion that Dr. Tortoriello and his colleagues have reached is that turmeric - and its active anti-oxidant ingredient, curcumin - reverses many of the inflammatory and metabolic problems associated with obesity and improves blood-sugar control in mouse models of Type 2 diabetes.

Type 2 diabetes is associated with chronic oxidative stress, a major contributor to cognitive decline and Alzheimer['s. Within 1 to 3 hours, a meal of mostly fatty foods seems to elevate free radicals, which] can damage tissue, including brain tissue.

'The new study “brings down the dose of resveratrol toward the consumption-reality mode"...Richard Weindruch...found that smaller doses, equivalent to the amount found in a glass of wine, may offer the same benefits [against aging and heart decline].'

'Intensive insulin therapy for a few days or weeks can drive [diabetes] into extended remission and at least partly restore β-cell function...[A] year later, the rate of remission among the patients given insulin was significantly higher...'