An interesting comparison of the cost of Lasik surgery vs that of contacts. Each carries its own risks, as indicated below.
Via: King Lasik
A personal blog discussing research, hope and healing for those with diabetes and insulin resistance.
An interesting comparison of the cost of Lasik surgery vs that of contacts. Each carries its own risks, as indicated below.
Via: King Lasik
We post a lot about fitness and exercise, including ways to exercise for the purpose of improving health and wellness. If you own a gym, work in the fitness industry or are connected to personal training, this information provides ways in which you can better support your customers (us).
Is there a relationship between what you eat and how you think? For example, do some foods influence your mood or enable you to learn more effectively? The relationship between mind, food and digestion is explored in the following.
Eating red meat comes with a risk according to a new study published in JAMA which correlated an increased risk of Type 2 Diabetes via a 20 year prospective study. Increasing the amount of rea meat consumption by just 0.5 servings per day was associated with a 48% increase in risk. A related editorial comments
The article by Pan et al1 confirms previous observations that the consumption of so-called red meat is associated with an increased risk of type 2 diabetes mellitus (T2DM). While previous studies have been cross-sectional in nature, the present study demonstrated that a relatively short-term (4-year) increase in red meat consumption is associated with subsequent risk, even in individuals who initially consumed low amounts of red meat. The authors demonstrated that consuming more red meat is also associated with weight gain, and a statistical adjustment for change in body weight attenuates but does not eliminate the risk, indicating that increased weight is not the only cause of a greater risk of T2DM associated with red meat consumption. The data in this article are valuable for those considering strategies to decrease the risk of developing T2DM.
I can see the Chick-vil-a commercial somewhere in all of this.
Nonnutritive sweeteners (NNS), such as sucralose, have been reported to have metabolic effects in animal models. However, the relevance of these findings to human subjects is not clear. We evaluated the acute effects of sucralose ingestion on the metabolic response to an oral glucose load in obese subjects…. These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS.
Subsequent news articles used these results in a highly speculative manner to hype a connection between the sweetener in Type 2 Diabetes which, in fact, was not part of the research.
Research aimed at treating diabetes through beta cells that can be transplanted just took a step forward:
Researchers at Washington University School of Medicine in St. Louis have identified a way to trigger reproduction in the laboratory of clusters of human cells that make insulin, potentially removing a significant obstacle to transplanting the cells as a treatment for patients with type 1 diabetes.
Efforts to make this treatment possible have been limited by a dearth of insulin-producing beta cells that can be removed from donors after death, and by the stubborn refusal of human beta cells to proliferate in the laboratory after harvesting.
They … used a novel conditioned medium expressing Wnt3a, R-spondin-3 and Noggin to engage Wnt signaling at the receptor level in combination with RhoA/ROCK inhibitors, SB-431542 and Y-27632, to significantly enhance adult human β-cell proliferation and maintain β-cell specific gene expression, insulin secretion and content in intact islets.
The new technique uses a cell conditioning solution originally developed to trigger reproduction of cells from the lining of the intestine.
“Until now, there didn’t seem to be a way to reliably make the limited supply of human beta cells proliferate in the laboratory and remain functional,” said Michael McDaniel, PhD, professor of pathology and immunology. “We have not only found a technique to make the cells willing to multiply, we’ve done it in a way that preserves their ability to make insulin.”
The findings are now available online in PLOS ONE. (A Novel Strategy to Increase the Proliferative Potential of Adult Human β-Cells While Maintaining Their Differentiated Phenotype)
The current method for harvesting human islets, which are comprised primarily of the insulin-producing beta cells, makes it necessary to find two or three donors to extract enough cells to produce an adequate supply of insulin to treat a single patient with diabetes.
The idea for the new technique came from an on-campus gathering to share research results. Lead author Haytham Aly, PhD, a postdoctoral research scholar, reported on his work with beta cells and was approached by Thaddeus Stappenbeck, MD, PhD, associate professor of pathology and immunology, who studies autoimmune problems in the gut. Stappenbeck had developed a medium that causes cells from the intestine’s lining to proliferate in test tubes.
“He said, why don’t you try it, and he gave us some samples,” Aly said. “We put the solution in our freezer for a month or so, and when we finally gave it a try, we were amazed at the results: human beta cells in Dr. Stappenbeck’s solution reproduced at a rate that was 20 times higher than beta cells in a solution that contained the sugar glucose.”
The ability to produce large quantities of human beta cells in the laboratory gives the researchers hope that they could one day be transplanted into patients with type 1 diabetes.
The advantage of Stappenbeck’s solution may be that it is designed to activate multiple growth signaling pathways in cells, according to the researchers. Earlier attempts to make beta cells proliferate focused on one or two growth pathways. The solution also activates genes that help prevent beta cells from dying.
Because pancreatic cancers are among the most deadly tumors, the scientists checked to make sure the proliferating beta cells weren’t becoming more like cancer cells. They found that none of the factors known to contribute to pancreatic cancer were active in the laboratory-grown beta cells.
“This is an important concern to keep in mind if we are to expand human beta cells in culture with this medium and subsequently transplant them into patients,” said Aly.
If the new availability of laboratory-grown beta cells makes it possible to treat patients with transplants from one donor instead of multiple donors, McDaniel noted, that might reduce the risk of immune system rejection of the transplants.
“Another benefit in using this novel growth medium to expand isolated human beta cells is that the cells remain healthier and have reduced levels of cell damage or death,” Aly said. “That may also reduce the chances of immune system rejection.”
In the United States, antibiotics are routinely given to animals that later find their way to the meat sections of virtually every supermarket. Animals are packed close together in crowded spaces and the drugs prevent the spread of disease. The predicted problem is the development of superbugs or bacteria that are highly resistant to current treatment options. Recent studies appear to have confirmed what scientists and nutritionalists have warned against:
A strain of the potentially deadly antibiotic-resistant bacterium known as MRSA has jumped from food animals to humans, according to a new study involving two Northern Arizona University researchers.
Paul Keim, Regents’ professor and director of NAU’s Center for Microbial Genetics and Genomics, and Lance Price, NAU faculty member and director of the Center for Food Microbiology and Environmental Health at the Translational Genomics Research Institute, collaborated with scientists at 20 institutions around the world on the study published today in the online journal mBio.
The TGen-led research utilized whole genome sequencing to study 89 genomes from humans and animals—including turkeys, chickens and pigs—with samples from 19 countries on four continents.
The research focused on methicillin-resistant Staphylococcus aureus CC398, also known as pig MRSA or livestock-associated MRSA because it most often infects people with direct exposure to swine or other food animals. It is likely that MRSA CC398 started as an antibiotic-susceptible strain in humans before it jumped to food animals.
After transferring to food animals, MRSA CC398 became resistant to two important antibiotics, tetracycline and methicillin, which are used for treating staph infections. The resistance likely is a result of the routine antibiotic use that characterizes modern food animal production. The animals commonly are given antibiotics to prevent infection and promote growth.
Keim, who also serves as director of TGen’s Pathogenic Genomics Division, said the study describes evolution in action. “The most powerful force in evolution is selection. And in this case, humans have supplied a strong force through the excessive use of antibiotic drugs in farm animal production. It is that inappropriate use of antibiotics that is now coming back to haunt us.”
Price, the study’s lead author, said the research was “like watching the birth of a superbug—it is simultaneously fascinating and disconcerting.” He said that while this strain of MRSA was discovered less than a decade ago it appears to be spreading very quickly.
“Our findings underscore the potential public health risks of widespread antibiotic use in food animal production,” Price said. “Staph thrives in crowded and unsanitary conditions. Add antibiotics to that environment and you’re going to create a public health problem.”
This is micro-evolution in action and provides a frightening look at the potential for health crisis and motivates an evaluation of our diet options.
Millions of Americans share your struggle to shed the extra pounds gained so easily in the age of fast and processed food, supersized proportions, and sugar laden beverages. We are a society that has uncovered the link between obesity and diabetes as a result of our prosperity and dietary indulgences.
Diets come and go and so does the weight. Rapidly losing pounds through radical and unsustainable diets inevitably fails and often leads to a return to the same or higher weight. In fact, over 90% of dieters regain lost weight within one year.
Experts have analyzed the situation and have lucid explanations for the yo-yo effect. I’m going to give you my opinion built only on my own experience.
First, short-term extreme dieting can’t be sustained and therefore does not lead to a change in eating, sleeping and exercise habits. The same behaviors that led to long-term weight gain return unless new patterns are formed. In particular, the use of food to deal with stress or as the basis for social interactions is deeply rooted and difficult to modify unless done in a purposeful manner with long-term health in view.
Second, crash dieting often involves severe calorie restrictions which leads to a reduced base metabolic rate (BMR), according to recent studies. In other words, your body automatically adapts to low calorie situations by using less energy. As a result, after an initial diet induction phase, often associated with rapid weight-loss, progress is slow. And, a return to former daily calorie intake may (I’m theorizing) lead to a greater energy imbalance resulting in rapid weight gain. The equation for fat gain looks something like: (calories stored as fat) = (consumed calories) – BMR – (calories used during activity). So, reducuing your BMR increases the likelihood of future weight gain if old habits return.
Short-term dieting for the sole purpose of weight loss is one dimensional and does not necessarily have long-term health as its objective. Weight or BMI may be associated with risk factors but these are not a comprehensive health metric. Overall health should be in view which may actually preclude some weight-loss strategies.
Over the past year I have had success that was built on a change in eating habits, a reduction in processed and fast foods, the introduction of sustainable exercise programs and consideration of sleeping patterns. I’m working on a post outlining the choices that were particularly helpful and some that were not… stay tuned.
I understand that maintaining a healthy weight following a successful weightless diet is difficult but this seems overly pessimistic:
Researchers claim that fat people, who lose weight either by dieting or exercising, will put it all back on again within a year.
The article does back off from the overarching generalization but claims that those of us who lose weight don’t have a chance to keep it off long term. Something tells me there is a great opportunity for a service industry to help dieters meet this daunting challenge. Anyone interested?
A few days ago a mentioned my one remaining nutritional vice. To be more accurate I should have said diet soda is/was my biggest vice. I’m now on day three w/out the aspartame laden beverage and not yet enjoying life w/out it. However, I am noticing a number of positives:
First, I’m saving the cost of several diet cokes including expensive impulse purchases at the check-out counter.
Second, it may be my imagination, but I simply don’t seem to be as hungry through-out the day.
Third, although I’ve replaced diet drinks with water, I’m not nearly as thirsty.
There’s nothing scientific about what I’ve written – it’s my anecdotal experience that began when two credible studies were reported that pointed out unintended physiological consequences of drinking diet softdrinks (and other products using aspartame).
I’m not sure I will remain diet soda free for life but want to give my current lifestyle change a couple of weeks.
As always, thanks for reading.
Kids and adults who eat candy tend to be …. thinner? How can that be?
Diet soda – not good for dieters (or anyone else)
In the every evolving world of medical research, reports that diet soda is linked to weight gain and increased fasting glucose level have periodically been reported. At the same time, contradictory articles suggest that as an alternative to sugar laden (fully leaded) soda, diet soft drinks have an advantage.
One of the reasons this topic interests me is that diet soda remains one of the few vices left in my daily nutritional regimen. Out of the picture are fast foods, deserts, simple carbs, chips, potato/French fries and alcohol. However, I partake in diet cola through-out the day.
New research is being reported at the 2011 American Diabetes Association’s Scientific Sessions by epidemiologists from the School of Medicine at The University of Texas Health Science Center San Antonio that suggests diet soda is no friend to those pre-disposed to Type 2 Diabetes:
In the constant battle to lose inches or at least stay the same, we reach for the diet soda. Two studies presented Saturday [June 25] at the American Diabetes Association’s Scientific Sessions suggest this might be self-defeating behavior.
Epidemiologists from the School of Medicine at The University of Texas Health Science Center San Antonio reported data showing that diet soft drink consumption is associated with increased waist circumference in humans, and a second study that found aspartame raised fasting glucose (blood sugar) in diabetes-prone mice.
To their statistically based results, the authors added comment and drama:
“Data from this and other prospective studies suggest that the promotion of diet sodas and artificial sweeteners as healthy alternatives may be ill-advised,” said Helen P. Hazuda, Ph.D., professor and chief of the Division of Clinical Epidemiology in the School of Medicine. “They may be free of calories but not of consequences.”
Here are the details
Human study: The San Antonio Longitudinal Study of Aging
To examine the relationship between diet soft drink consumption and long-term change in waist circumference, the Health Science Center team assessed data from 474 participants in the San Antonio Longitudinal Study of Aging, or SALSA. This is a large, population-based study of the disablement process in elderly Mexican Americans and European Americans. Dr. Hazuda, senior author of the presentation, is SALSA’s principal investigator and has led the study for two decades.
Measures of height, weight, waist circumference and diet soda intake were recorded at SALSA enrollment and at three follow-up exams that took place over the next decade. The average follow-up time was 9.5 years. The researchers compared long-term change in waist circumference for diet soda users versus non-users in all follow-up periods. The results were adjusted for waist circumference, diabetes status, leisure-time physical activity level, neighborhood of residence, age and smoking status at the beginning of each interval, as well as sex, ethnicity and years of education.
Diet soft drink users, as a group, experienced 70 percent greater increases in waist circumference compared with non-users. Frequent users, who said they consumed two or more diet sodas a day, experienced waist circumference increases that were 500 percent greater than those of non-users.
Abdominal fat is a major risk factor for diabetes, cardiovascular disease, cancer and other chronic conditions. “These results suggest that, amidst the national drive to reduce consumption of sugar-sweetened drinks, policies that would promote the consumption of diet soft drinks may have unintended deleterious effects,” the authors wrote.
Co-authors include Sharon P. Fowler, M.P.H., faculty associate, and Ken Williams, M.S., P.Stat., adjunct assistant professor and biostatistician, in the Division of Clinical Epidemiology.
Mouse study: Aspartame consumption in diabetes-prone mice
In the related project, Ganesh Halade, Ph.D., Gabriel Fernandes, Ph.D., the senior author and professor of rheumatology and clinical immunology, and Fowler studied the relationship between oral exposure to aspartame and fasting glucose and insulin levels in 40 diabetes-prone mice. Aspartame is an artificial sweetener widely used in diet sodas and other products.
One group of the mice ate chow to which both aspartame and corn oil were added; the other group ate chow with the corn oil added but not the aspartame. After three months on this high-fat diet, the mice in the aspartame group showed elevated fasting glucose levels but equal or diminished insulin levels, consistent with early declines in pancreatic beta-cell function. The difference in insulin levels between the groups was not statistically significant. Beta cells make insulin, the hormone that lowers blood sugar after a meal. Imbalance ultimately leads to diabetes.
“These results suggest that heavy aspartame exposure might potentially directly contribute to increased blood glucose levels, and thus contribute to the associations observed between diet soda consumption and the risk of diabetes in humans,” Dr. Fernandes said.
These two translational research studies resulted from collaboration between Fowler and Drs. Hazuda and Fernandes and their research teams. The Institute for the Integration of Medicine and Science (IIMS) funded the work. IIMS is the Health Science Center entity that oversees the university’s Clinical and Translational Science Award (CTSA), a National Institutes of Health-funded program to encourage the rapid translation of scientific discoveries from the laboratory through the testing process and to practical application for the health of communities.
I’m not a medical expert in the field but wonder if (1) there are assumptions related to outcomes revealed by the following, “might potentially directly contribute” and “may have unintended deleterious effects”. In addition, the human study did not establish causality or an underlying mechanism which would conclusively reveal diet soda consumption causes weight gain (or waist circumference increase).
Never-the-less, it does seem clear that there is a strong relationship between obesity and diet soda and that there is an unintended physiological response associated with aspartame consumption that is both unintended and undesirable.
Now, will this lead to a change in your consumption of diet soda?
As for me, I’m going to eliminate the drink from my diet and report back to you the impact.
After the early start-up days, Google, like many larger companies, has struggled with adjacent markets. The company missed the boat on social media and GoogleWave was a disaster. That said, their indexing and search, translation, mail, online office, webmaster tools, advertising and VOIP are best in class.
I think it is healthy for a tech company to fail once in a while… it shows their willingness to take chances, etc. rather than acquire (and stagnate) successful start-ups.
An artificial pancreas, as commonly reported, is a medical device that is worn and attached to a person. It autonomously changes the insulin administered to a person with diabetes in response to glucose measurements, which are measured automatically.
The system has a few basic components that include a continuous glucose monitor (CGM), a continuous subcutaneous insulin pump and a control system that determines the rate of insulin infusion given the measured glucose through time. An artificial pancreas will also include a display, communication system, overrides, alarms, fail safes, and controls for user input (i.e., for indicating meals, exercise, etc). However, the fundamental components are the three I mentioned.
Despite decades of research, the three basic components as a whole may not be ready for complete autonomous application. Insulin pumps are quite reliable and control algorithms have reportedly been developed that effectively achieve a target range while avoiding hypoglycemia. However, continuous measurement of blood glucose through current subcutaneous sensing technology has proven to be quite challenging .
That said, researchers are now entering what appears to be the final stretch to bring an artificial pancreas (or a system that at least reduces insulin in response to low glucose) to the FDA…. And, we want it:
Teenaged delegates from the Juvenile Diabetes Research Foundation testified on Capitol Hill, urging Congress to accelerate research and review of artificial pancreas systems for managing insulin for patients with type 1 diabetes.
“After participating in clinical research since I was three years old, I can honestly say the closed loop artificial pancreas trial was the most amazing experience of my entire life and holds so much promise for people living with this disease,” said Kerry Morgan, a 17-year-old JDRF Children’s Congress delegate from Glen Allen, Va., who testified before the Senate Committee on Homeland Security and Government Affairs this week.
Would you be surprised to learn that the FDA wants it too:
FDA WANTS APPROVAL, TOO
Charles “Chip” Zimliki, chairman of the U.S. Food and Drug Administration’s Artificial Pancreas Critical Path Initiative, which was created in 2006 to accelerate the availability of an artificial pancreas system, says he is eager to have a system approved.
“The FDA wants the artificial pancreas on the market as much as anyone else does. We just have to operate within U.S. laws to make sure it is safe and effective,” Zimliki said.
Last week, the agency released guidance for how to develop a low glucose suspend system, an automatic shut-off mechanism used with an insulin pump. Medtronic already sells pumps with this the feature in Europe. It safeguards against a dangerous drop in glucose levels by temporarily halting glucose delivery.
By year-end, FDA plans to release detailed guidance on more complicated closed-loop systems, Zimliki said.
“We think of this system, the artificial pancreas, as one unit. There is going to have to be agreement among various companies to determine who is the reporting party for submitting it,” he said.
“That is a relatively new idea with respect to these systems.”
Zimliki, who is a type 1 diabetic, thinks the first approved devices will be ones that deliver insulin only, but he is very encouraged by the system being developed by the team at Boston University and Massachusetts General.
“They have what I call the Cadillac of closed-loop systems,” he said. In addition to delivering insulin, the device also delivers an infusion of glucagon, a hormone released by the pancreas to raise blood sugar levels.
“They are showing some very promising results,” he said.
Diabetes Mine has an interesting post and interview with the principle investigators from Boston University and Massachusetts General Hospital (see the youtube video).
In case you haven’t already heard, researchers are now reporting that Type 2 Diabetes may (possibly) be reversed by a restricted low-calorie diet:
Adhering to the strict 600 calorie-a-day diet causes fat levels in the pancreas to plummet, restoring normal function, found Prof Roy Taylor of Newcastle University.
The discovery, a “radical change” in understanding of the condition, holds out the possibility that sufferers could cure themselves – if they have the willpower.
Until recently received medical wisdom was that Type 2 diabetes was largely irreversible.
But this small-scale study indicates that defeating it could be easier than commonly thought.
Prof Taylor asked 11 volunteers, all recently diagnosed, to go on what he admitted was an “extreme diet” of specially formulated drinks and non-starchy vegetables, for eight weeks.
As the article goes on to point out, the trial study involved only 11 patients that ate a “meal-replacement” milkshake of 150 calories three times a day. This was supplemented with three portions of non-starchy vegetables including cabbage, broccoli, peppers, tomatoes, cucumber and lettuce. After one week, their pre-breakfast blood sugar levels had returned to normal and an MRI scan revealed that the fat levels in the pancreas were also normal, down from around eight per cent to six per cent.
Notes to self:
While complications of diabetes are understood and have been tied to the cost of providing healthcare, trends indicate the incidence Diabetes Mellitus in the United States and other developing countries is growing at an alarming rate.
There is so much about diabetes that is understood, predicted and recommended and yet management continues to be a challenge. Could it be that better tools are needed?
To meet the challenge, researchers have been developing technology based tools that will help manage the disease through automation. That is, automatically administering an appropriate amount of insulin in response to a person’s glucose level and carbohydrate intake.
Often called the “artificial pancreas”, such systems combine continuous glucose measurement systems (CGM), insulin pumps (giving continuous subcutaneous insulin infusion) and advanced algorithms to give insulin dosing recommendations and stop infusion when a hypoglycemic event is predicted. The latter is called a “low glucose suspend” (LGS) device and provides benefit as a result of its autonomous action aimed at avoiding low blood sugar (predictively) or reducing the impact of hypoglycemia in a reactive manner.
Yesterday, the FDA release a new guidance document that will help medical device manufacturers submit their artificial pancreas-like product for review. The move is encouraging for a number of reasons. First, the agency is agreeing that automation has a role in the marketplace and is encouraging a path forward. Second, progress has been made and interest expressed to the point that the FDA felt is necessary to invest in guidance.
On the other-hand, there are a number of challenges the agency suggests must be remedied involving CGMs:
But are they effective enough to “pause” an insulin infusion? Perhaps, but what if users begin to rely on a “pause” as their safety net even though CGMs have the issues listed above?
From an altruistic standpoint, advances in this area will help those suffering from Diabetes and in particular individuals who are unable to properly treat their disease (esp. children). From a business stand-point, a revolutionary product that is intuitive, effective and safe will provide a huge advantage in a market that seems stuck on the stick meter.
A recent study, appearing in Nature Magazine, showed that an antibody called anti-CD20, which targets and eliminates mature B cells in the immune system, stopped diabetes type 2 developing in lab mice prone to develop the disease, and restored their blood sugar level to normal:
Chronic inflammation characterized by T cell and macrophage infiltration of visceral adipose tissue (VAT) is a hallmark of obesity-associated insulin resistance and glucose intolerance. Here we show a fundamental pathogenic role for B cells in the development of these metabolic abnormalities. B cells accumulate in VAT in diet-induced obese (DIO) mice, and DIO mice lacking B cells are protected from disease despite weight gain. B cell effects on glucose metabolism are mechanistically linked to the activation of proinflammatory macrophages and T cells and to the production of pathogenic IgG antibodies. Treatment with a B cell–depleting CD20 antibody attenuates disease, whereas transfer of IgG from DIO mice rapidly induces insulin resistance and glucose intolerance. Moreover, insulin resistance in obese humans is associated with a unique profile of IgG autoantibodies. These results establish the importance of B cells and adaptive immunity in insulin resistance and suggest new diagnostic and therapeutic modalities for managing the disease.
One of the many reasons that this is significant is that it could lead to future novel treatments.
We post a lot about fitness and exercise, including ways to exercise for the purpose of improving health and wellness. If you own a gym, work in the fitness industry or are connected to personal training, this information provides ways in which you can better support your customers (us). Via: iContact
Is there a relationship between what you eat and how you think? For example, do some foods influence your mood or enable you to learn more effectively? The relationship between mind, food and digestion is explored in the following. Via: Renewlife Probiotic Supplements