Does 5.5 A1c Predict Retinopathy?

A new, high quality study which I cited in my Updates to Blood Sugar 101 blog found a steep increase in the incidence of retinopathy in people not diagnosed with diabetes whose A1cs were 5.5% or more. The study found that the predictive value of the A1c was much stronger than the predictive value of fasting blood sugars in the same population.

At first glance this might be a very disturbing finding to those of us who find it difficult if not impossible to lower our A1cs below 5.5%. I have not been able to do this even when eating a very low carb diet. My A1cs are almost always between 5.7% and 5.8%.

I've discussed why some of us have higher than expected A1cs in another blog post.

But I want to raise another point here, one that is often lost when researchers use A1c:

The A1c reflects average blood sugar values over time, but there are many ways to attain an average.

In fact, what the A1c really measures the amount of glucose that has gotten bonded onto red blood cells over a period of time. The more exposure red blood cells have to high blood sugars, the more glucose they accumulate. Since these red blood cells live about 3 months, the A1c is supposed to reflect three month's worth of blood sugar exposure. In reality, though, the A1c reflects the several weeks right before the test, much more than it does the whole three month period.

Studies that compare CGMS readings with A1cs conclude that that A1c gives a close approximation to average blood sugars for a population as a whole, and much rougher approximations for the average blood sugar of the individuals in a population.

Note, however, that people with unusually high or low concentrations of red blood cells will get A1c readings that do not reflect the actual concentration of glucose in their blood. So will people whose red blood cells have longer than normal lives and those with certain genetic oddities that affect their red blood cells' ability to bond to glucose.

But even in people with absolutely typical red blood cells, two people with the identical A1c can achieve those A1cs while experiencing very different patterns of daily blood sugar fluctuation.

For example, a 7% A1c has been most recently equated with an average blood sugar of 155 mg/dl (8.6 mmol/L). A person can achieve this average by maintaining blood sugars that oscillate between 85 mg/dl (4.7 mmol/L) before meals and 225 mg/dl (12.5 mmol/L) after meals or they can get the same A1c by maintaining a blood sugar that oscillates between 130 mg/dl (7.2 mmol/L) and 180 mg/dl (10 mmol/L). Depending on which pattern they follow, the likelihood of developing diabetic complications is very different.

This was clearly demonstrated by the comparison of two studies--the UKPDS and the Kumamoto Study--where participants had the same 7% A1c but very different complication profiles because their post-meal blood sugars were very different. You can find the citations to the comparison of these studies HERE.

So before we panic about the finding that as A1cs go over 5.5% the incidence of retinopathy spikes upward, we need to give some thought to what the underlying blood sugar fluctuations might have been of the people with 5.5% and greater A1cs in this population.

An A1c of 5.5% corresponds (in large populations) with an average blood sugar of 112 mg/dl (6.2 mmol/L).

Since this group was made up of people not diagnosed with diabetes, we can make a pretty good guess at what kind of diet they were eating: One very high in carbohydrates. Remember, nutritionists consider 300 grams a day a normal carbohydrate intake.

It is likely some of these "normal people" who were prediabetic. In that case, they were likely to be experiencing very high post-meal numbers that dropped back to normal after two hours or even went low, as happens with reactive hypoglycemia. If that were true, they would be were seeing oscillations that veered between 75 and 150. The average of these two values just happens to turn out to be 112 mg/dl.

We already know that exposure to post meal blood sugar levels of 140 mg/dl (7.7 mmol/L) is associated with a rise in many different diabetic complications. So it no longer is mysterious why that 5.5% A1c might be the lower boundary after which retinopathy diagnoses start to rise steeply. Those "normal" people with the 5.5% and higher A1cs were probably eating high carbohydrate meals throughout the day and spending hours each day above that 140 mg/dl threshold that is already
documented as the level at which diabetic complications start to ramp up.

The graph showing normal people's blood sugars, which you will find HERE, shows that there is a significant proportion of "normal" people who are going up over 140 and staying there for almost 2 hours after eating their normal high carb breakfast. They are likely to do this every day and probably see similar patterns after lunch and dinner too. My guess is that it is these "normal" people who are most likely to developing diabetic complications in the prediabetic range that corresponds to A1cs at and above 5.5%.

But there is another blood sugar pattern that also leads to that 5.5% A1c--the pattern in which the blood sugar stays near 112 all day long, or perhaps where there is a relatively high fasting blood sugar--110 mg/dl, and very narrow fluctuations at meal time, perhaps up to 120 and then back down to 90.

This is the pattern characteristic of people who control their blood sugar by cutting way back on carbohydrates and using drugs like metformin and/or insulin to flatten out their blood sugar peaks. Many find that they cannot prevent higher than normal fasting blood sugars, but they can easily keep their blood sugar under 120 mg/dl after meals.

For people who achieved a 5.5% A1c--or even one slightly higher--by keeping their blood sugars under 140 mg/dl most of the time, the risk for retinopathy may well be much lower.

None of the published large scale studies links complications to post-meal blood sugars because post-meal numbers are too expensive to monitor in a large group, so it is impossible to prove this, but anecdotal reports from those of us in the online diabetes community who have kept our blood sugars under 140 mg/dl for years at a time suggest this is true.

So if you can keep your A1c under 5.5%, you can feel confident that you are doing what you need to do. If you can't, you are in the majority of people with diabetes and there is no need to panic if you keep track of your post-meal highs and keep them under 140 mg/dl as much as possible. (The technique described HERE will help you do just that.)

And if you do go high from time to time--and we ALL do--don't panic. It takes many hours spent at high blood sugar levels day after day, month after month, over a period of years that promote complications. If you spike high for an hour or two every now and then, it is not likely to cause massive damage.

 

Antioxidant Vitamins Raise Insulin Resistance and Render Exercise Useless

Nothing has been dearer to the hearts of nutritionists than antioxidants. The concept, like all concepts promoted by nutritionists, is easy to understand. Oxidation is the highfaluting word for what happens when things rust. So taking the antioxidant vitamins, Vitamin C and Vitamin E is supposed to "keep your body from rusting."

Except it doesn't. A slow trickle of bad news has been coming through over the past couple years linking antioxidants with bad outcomes.

The first finding came from a large scale study conducted in England where half of 20,536 people considered high risk for heart disease took vitamin C,E, and beta-carotene supplements and half didn't. It found no difference at all in the rates of heart attack, other signs of cardiovascular disease, cancer or, indeed, hospitalization for any other cause.

Then a February 2007 study found that antioxidant supplements actually seemed to raise the risk of death in those who took them.

Yet another blow was dealt to the idea that antioxidants were helpful by the results of the Physicians Health Study II published in 2008. In this double blind, placebo controlled study of 14,641 male physicians taking Vitamin C or E or a placebo that lasted a decade, the conclusion was, " neither vitamin E nor vitamin C supplementation reduced the risk of major cardiovascular events." Not only that, but "...vitamin E was associated with an increased risk of hemorrhagic stroke."

However, there was some hope that supplementing with these vitamins might be of some use specifically in people with diabetes after studies showed that the beta cell was uniquely vulnerable to oxidative stress because it is poor in the production of antioxidant substances.

A paper published in 2000 that analyzed results of the large scale EPIC-Norfolk study seemed to suggest this was true. It found that the higher the plasma vitamin C level in the 6,458 people they studied, the lower their hba1c seemed to be.

But the question was whether the high level of vitamin C actually caused the lower blood sugar levels, or whether its presence was a marker for something else--for example a diet low in junk food.

A further analysis of EPIC Norfolk data published in 2004--after the early results were in suggesting he ineffectiveness of vitamin supplementation against heart disease, pointed to the latter explanation. The study title says it all: Occupational social class, educational level and area deprivation independently predict plasma ascorbic acid concentration: a cross-sectional population based study in the Norfolk cohort of the European Prospective Investigation into Cancer (EPIC-Norfolk) Shohaimi S, Bingham S, Welch A, et al. Eur J Clin Nutr, Mar 31 2004, e-pub.

Why drag this up again? Because two very intersting studies that came out this past year cast some light on WHY antioxidants may be bad for us.

The first is this study, available in full text:

Antioxidants prevent health-promoting effects of physical exercise in humans Michael Ristow et al. PNAS May 26, 2009 vol. 106 no. 21 8665-8670 doi: 10.1073/pnas.0903485106

The researchers in the PNAS study found that "Exercise increased parameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals."

Why? A rodent study conducted by Tony Tiganis and published in Cell Metabolism in October of 2009 [full text available online as of Oct 25, 2009] found that high doses of antioxidants may interfere with cellular processes in a way that increases insulin resistance.

Reactive Oxygen Species Enhance Insulin Sensitivity" Kim Loh et al. Cell Metabolism,Volume 10, Issue 4, 260-272, 7 October 2009, doi:10.1016/j.cmet.2009.08.009

To read a description of this study in layman's terms view:
Reuters: Antioxidants may increase diabetes risk

Since it is a mantra repeated throughout Diabetes research that ROS are strongly associated with the damage done by diabetes to our organs, after reading this we find ourselves scratching our heads.

We are told to exercise, but this research suggests exercise is only effective in reducing insulin resistance when antioxidants are not present and ROS are produced.

So what message should we take from this? My guess is that it suggests we should confine our intake of antioxidant vitamins to those that come bound up with foods that have long made up a normal part of the human diet. These foods contain very modest doses of antioxidants.

The studies finding problems with antioxidants all use large doses of supplemental vitamins. It is likely that the amount of Vitamin C in your veggies and the Vitamin E in your sunflower seeds is low enough to avoid overwhelming cellular processes like lab created vitamins do.

Rust is not the only example of oxidation in our environment. There is also flame. And when you are trying to burn nutrients, maybe a bit of oxidation is good for you.

 

Gestational Diabetes

I frequently receive emails asking me about Gestational Diabetes (GD), which is the term used for diabetes that is diagnosed only after a woman, previously considered normal, displays abnormal glucose tolerance test results during pregnancy.

Because obstetricians do a very good job of diagnosing and treating GD, I have not discussed it on my web site. If you are pregnant and have GD your doctors are almost certain to give you insulin to normalize your blood sugars. The blood sugar targets given pregnant women are much lower than those given the average person with Type 2 diabetes--low enough to ensure health. Follow them and you should avoid the problems associated with GD that were suffered by those of us whose GD was not well treated in the past.

Some women have found the chat boards at Diabetic Mommy helpful for finding support.

The real problems with GD only start after you give birth to your baby and bid goodbye to your obstetrician. Why? Because the average family doctor still appears to believe that GD is nothing more than one of the many complications of pregnancy and that if your blood sugar returned to "normal" after delivery, you need do nothing else.

The problem here is that the family doctor is all too likely to define "normal" as meaning "having an A1c under 7%" or, if he's a bit better educated 6.5%. Perhaps he won't even run an A1c test but will merely send you for a fasting glucose test. If the result comes back under 125 mg/dl, he may tell you you "aren't diabetic" and that will be that.

Unfortunately, if you have experienced a diabetic pregnancy, "that" is far from that. Because no matter how "normal" your doctor may tell you you are, you would not have developed GD unless your ability to secrete insulin was so borderline, before you started your pregnancy, that the stress of adding your baby's metabolic demands to that of your own organs exhausted it.

Relieving this stress by giving birth to your baby may return you to your previous state--but even if it does, the fact that you had GD should make you realize that your blood sugar control is only marginal, and this means that any other stressor might well push you back into full fledged diabetes.

What are those stressors? There are many.

1. Environmental pollutants that increase insulin resistance or damage the beta cells. These can include exposure to pesticides and industrial chemicals. Atrazine--a commonly used herbicide has been linked to increased insulin resistance. Arsenic, which is given off by power plants, has also been linked to diabetes. So have PCBs.

2. The use of FDA approved medications known to raise blood sugar or increase insulin resistance. These include cortisone treatment--either injections or prednisone pills, most SSRI antidepressants and the atypical antipsychotic drugs.

If you wonder if a drug you are taking can stress your blood sugar control, download the official FDA "Prescribing Information" by googling the name of the drug and the words "Prescribing Information" and look in the "Side Effects" section of the Prescribing information for the word "hyperglycemia." Drugs known to cause weight gain also may cause the same kind of stress to your marginal insulin production capacity.

You can find links to the studies that discuss environmental and pharmaceutical causes of insulin resistance and diabetes HERE

3. Gaining more weight. Though weight gain is often the result, rather than the cause of insulin resistance, if your weight gain results from overconsumption of fructose and eating a high carbohydrate diet, even a low fat one, some of your new weight is likely to be intracellular liver fat, which has only recently been recognized as a significant cause of increased insulin resistance. Carbohydrates not dietary fat turn out to be what raises the triglycerides that get deposited in the liver.

4. Autoimmune attack on the beta cells of the pancreas. A small but significant proportion of those who develop GD suffer from LADA a slow developing form of autoimmune diabetes. These people may experience a slight improvement in their blood sugars after they give birth, but over time their ability to secrete insulin will decline because there is currently no way to halt this kind of autoimmune attack.

What Can You Do?

The best approach to take if you have experienced a diabetic pregnancy is this. Once every month or two, test your blood sugar at home after meals. If you can't afford the expensive prescription strips, use the cheaper strips and meter sold at Wal-Mart under the "Relion" brand.

If you see values over 140 mg/dl one hour after eating, test more frequently. Blood sugars routinely going over 140 mg/dl are capable of damaging your beta cells leading to full fledged diabetes. Even with out diabetes blood sugars in the "pre-diabetic" range have been shown to be capable of giving you the early diabetic complications.

If you see blood sugars over 140 mg/dl an hour or more after you eat, cut back on carbohydrates using the advice you will find here:

How To Get Your Blood Sugar Under Control

Cutting back on carbohydrates is usually all most people need to regain normal blood sugars, even those who have been given diagnoses of Type 2 diabetes.

When Diet Might Not Work

If you were thin when you became pregnant and still developed Gestational Diabetes--or if you developed GD very quickly after becoming pregnant no matter what your weight, your situation may be more complex. Pregnancy often gives the first sign that a person may have one of the rarer forms of diabetes often called "Type 1.5." If you think this might be the case, read these pages:

LADA - Slow Onset Type 1 Diabetes With Some Type 2 Features

MODY - It's Not Type 1 or Type 2 But Something Else

Before you attempt to diagnose yourself, please be aware that MODY is much, much rarer than LADA. But the incidence of LADA appears to be increasing swiftly as part of the whole society-wide explosion of autoimmune disease and if you have any other autoimmune disease in the family, or have relatives diagnosed with Type 1 diabetes the chance you might have a rare form of "Type 1.5" goes way up.

It is also worth noting that while most overweight people who get GD are most likely to move on to an ultimate diagnosis of "Type 2" diabetes, overweight people also can develop autoimmune diabetes. Unfortunately, doctors often assume any overweight person must have Type 2 diabetes and do not run the tests that could diagnose LADA. No matter what you weigh, if your "Type 2 diabetes" continues to deteriorate, does not respond to oral drugs or to cutting carbohydrates, it may not be Type 2 diabetes at all.

Since LADA requires a very different kind of treatment than regular Type 2, this is significant. Oral drugs will not correct LADA and over time a person with LADA who is not given insulin can end up in the emergency room in a dangerous state called "Diabetic ketoacidosis" that happens when the pancreas stops making insulin.

So if you have had a diabetic pregnancy, and afterwards your blood sugars continue to rise, even if you cut way back on carbohydrates--especially if you have a family or personal history of other autoimmune-related disorders, such as authoimmune Thyroid disease or rheumatoid arthritis--insist that your doctor test you for the antibodies associated with Type 1 diabetes to see if you actually have LADA.

If your family doctor isn't familiar with LADA--and many are not--insist on seeing an endocrinologist, ideally one associated with a large hospital that has a medical school.

Most women who were diagnosed with GD in mid pregnancy probably do have the genetic makeup that over time leads to the development of Type 2 Diabetes. If this is your situation, and you see abnormal blood sugars after eating, you will respond strongly to cutting back on your carbohydrate intake.

And because you got warning of borderline high blood sugars early, you can rejoice because you have been given a golden opportunity to prevent your diabetes from progressing because GD gave you the warning which let you catch oncoming Type 2 diabetes very early, before it has been given a chance to ravage your organs.

Aggressive control with diet and modest exercise, aided, perhaps by metformin, if your doctor will prescribe it to you, should keep your blood sugars in the normal range for decades.

You also will want to feed your children diets that are not high in carbohydrates because chances are if you don't handle them well, neither will they. Teaching them that each meal does not have to start with bread, continue on with potatoes, and end with dessert can go a long way to helping them stay metabolically normal no matter what genes they have inherited.

 

Only Christians Get Type 1 Diabetes?

The JDRF just sent me one of those mailings that makes me question whether to send them another dime.

You know the kind I mean--the ones that contain expensive "gifts" intended to guilt you into sending them a bigger contribution, but which, if you have already sent a contribution or two, make you wonder why your money went to buy greeting cards or stickers and expensive postage for oversize envelopes instead of funding research that might help people with Type 1 Diabetes.

I get a lot of these expensive mailings from the JDRF and they are turning me off to the organization.

This one was more annoying than usual, because it contained a big fat pack of Christmas cards. And I mean "Christmas" cards. Red and green with text and imagery that even on the cards that did not use the "C" word still made them unsuitable for sending to people who aren't Christian.

So I came away wondering why the JDRF's fundraising geniuses decided to send out a fundraiser that carries the subtext that people who do not celebrate Christmas need not feel guilty for not sending them money. Bad move folks!

But least they didn't send out candy cane stickers like the ADA does every year. Which reminds me it's time to remind you that before you respond to the American Diabetes Association you should check out what percentage of your dollar will go into "activities"--in California it may be less than 33% elsewhere not much better. The Charity Navigator gives them the very lowest ranking possible--one star out of four.

The ADA raised $213,464,233 last year. That's a lot of money. It does NOT fund its journals which are subscription only and very expensive--and which researchers must pay to get their studies published. Did it fund direct research? No. Because that isn't the ADA's mission.

So where did that money go? Good luck in finding out. Perhaps it went into printing and distributing flyers telling people to eat healthy whole grains, pasta and bananas or urging them to keep taking Avandia until more studies are done. That's the main "educational" message I've seen from the ADA over this past year. And of course it must be expensive gearing up to put "Diabetes friendly" labels on low fat boxed breakfast cereals--that's the ADA's next big "breakthrough".

 

Utterly Flawed Research Claims a Spurious Benefit for Mangosteen

Every now and then a piece of nutritional research crosses my desk that is so poorly conducted that I can't resist the temptation to post it here and use it as an example of how people who are supposed to be scientists degrade themselves in the pursuit of results that will please their corporate sponsors.

The study can be read in all its glorious full text awfulness here:

Evaluation of Mangosteen juice blend on biomarkers of inflammation in obese subjects: a pilot, dose finding study. Jay K. Udani. Nutrition Journal 2009, 8:48, doi:10.1186/1475-2891-8-48

The way this study is being reported in the media can be seen here:
Science Daily: Mangosteen Juice Could Protect Health In The Obese

So what's wrong with this study? Let's take a closer look.

The abstract of the study says "The purpose of this study was to evaluate the effect of multiple dosages of a proprietary Mangosteen Juice blend on indicators of inflammation and antioxidant levels in obese patients with elevated C-reactive protein (CRP) levels." Okay, that sounds reasonable.

So let's look at the methodology. Forty-four people were given tests of inflammatory markers like CRP. These were "screened" out of an original population of 122 people, though the researchers don't tell us what they were screened for.

These people were broken into four groups. Three of the groups were told to drink a branded mangosteen juice product twice a day, each group drinking it in different sized doses. The fourth group were given a placebo to drink, though we are not told what size dose they were given. So far this sounds reasonable.

But when you red the full text description of what the subjects were actually given to drink you see at once that the Science News report title is flawed. Because the researchers didn't really give any of their subjects mangosteen juice. Instead they gave them a branded "mangosteen juice blend" where only the "primary ingredient" was mangosteen juice.

And they had no idea what percentage of the juice blend was mangosteen, because the branded juice blend also contained:

apple fruit juice, pear fruit juice, grape fruit juice, pear fruit puree, blueberry fruit juice, raspberry fruit juice, strawberry fruit juice, cranberry fruit juice, and cherry fruit juice.

Now the way that the FDA defines a "primary ingredient" all something has to do to be listed first on the label is to make up a greater percentage of the total of the food in question than the ingredients that follow it.

So since this product contains 9 other juices or purees, the mangosteen might easily make up only 11% of the juice, while each of the other ingredients made up 9 or 10% of the product.

So whatever benefits the study found for the blend, it tells us little about the effects of mangosteen juice, because the substance being tested is probably 90% other juices, several of which--blueberry, raspberry, and cranberry juice have already been found to have very slight health effects (though probably the research that "prove" those benefits isn't much stronger than this research.)

Now let's look at the placebo: Here's how it is described.

The placebo consisted of water, sucrose (3 g/30 ml), citric acid, red grape juice concentrate, fiber complex, grape skin, natural flavors, red #40, cloud (ester gum), whey protein isolate, sodium benzoate, xanthan gum, blue #1, and caramel color.

Is a sugar water solution with a fruit juice NOT found in the other juice mixture, whey protein, artificial colors, and preservative a true placebo when compared with a mix of fruit juices?

It is very possible that any difference attributed to the mangosteen juice blend--which more honestly should have been called a blend of "standard fruit juices and puree with a touch of mangosteen"--might only be due to the fact it didn't contain sucrose, whey protein, or the chemical additives in this bioactive "placebo."

But let's move on. The conclusions section reports,

HS-CRP measurements dropped after 8 weeks treatment compared to baseline in all 3 dose groups and increased in the placebo group. The changes from baseline were not significant but the comparison of change from baseline was significant for the 18oz group when compared to placebo (p=0.02).[emphasis mine]

Other markers of inflammation (inflammatory cytokines) and a marker for lipid peroxidation (F2 Isoprostane) did not show any significant differences when compared with placebo. There was a trend towards a decrease in BMI in the juice groups.

Either I'm missing something here, or the conclusion of this study was that there were no real, or at least statistically significant differences found between the three groups drinking the juice and the placebo juice. Statistically, the results of the study could have been the result of chance.

But because the researchers needed to find proof that their sponsor's product worked--did I mention that the study was sponsored by the maker of the branded juice--they looked for some way to turn insignificance to significance, and they found it by computing the average change from baseline and glory be, this statistic derived from a meaningless statistic turned out to achieve statistical significance in the one groups of mangosteen blend drinkers that drank the largest dose.

But wait, let's look a little more closely at the make up of the three groups of juice drinkers. There were 9 people in the group whose change from baseline rose to statistical significance, which is a very small number. In contrast, there were 11 people in the group that drank the lowest dose of juice and 12 in the group that
drank the middling dose. Only 8 people were in the control group.

This is a lot of variance. It makes me think any statistically valid comparison between the groups highly suspect, especially when what is being compared is the statistic involving both mean and standard deviation which start to lose meaning as the size of the groups compared gets smaller.

Let's have a look at that standard deviation. That's the statistic that shows us the extent to which individual values clustered around the average. The smaller it is, the closer the clustering. As it turns out, the standard deviations seen in the "change from baseline" were very large: the average was 0.90 but the standard deviation was a whopping ± 9.5 [no units given] for the placebo group. The decrease in the one group that supposedly rose to significance was an average of -1.33 with a ± 3.0 standard deviation.

Hmmmmmm......

But, though by now you might think it couldn't, it gets worse. Because lets look closer at the groups involved. How well matched were they?

As it turns out, not very. The placebo group's average age was 45. The average ages of the groups drinking the juice were 52, 33, and 50. Given that the measures of inflammation being measured are very age sensitive, comparing groups of significantly different ages appears to invalidate the idea that what we had here was anything approaching a properly designed controlled trial. The measures of "obesity" were not very well matched either.

The description here claims that BMI and body fat percentage "trended downwards." This is backed up with Table 2 which to the eye that has any experience with the way weight fluctuates over the eight week period of this study, makes it clear that the "trend" was only in the mind of the hopeful sponsor. In fact, using the selective technique used by these researchers, we could say that the Placebo "trended" towards achieving weight loss benefits. But of course, it didn't any more than the juice because this study has by now completely lost any claim to being scientifically useful.

The study abstract concludes by stating

..a proprietary mangosteen juice blend (XanGo Juice) reduced CRP levels (increased change from baseline) compared to placebo for those taking the highest dose of 18 oz. per day. Further studies with a larger population are required to confirm and further define the benefits of this juice.

Only in the full text did the researchers tell the truth when they added,

... the use of multiple comparisons in the analysis of the study data increases the risk of statistical error resulting in a false positive.

In fact, these researchers failed to tease a convincing false positive out of anything but that pathetic "change from baseline" statistic used to amplify a statistically meaningless finding into one they could pawn off on a credulous public as a significant one. One wonders how they could have the nerve to suggest that "further studies are required to confirm and further define the benefits of this juice."

Could it be that the sponsor likelihood of sponsoring (i.e. paying for) further research had anything to do with it?

I'll leave you to determine that.

But really, the gall of the people who come up with this stuff. And the further gall of the journals that publish it, knowing that most people will only look at the abstract or the news report that will undoubtedly appear in the magazines and web sites supported by supplement sellers.

You can expect to see the hucksters using this "research" to prove that mangosteen has miraculous health giving effects. And the poor obese schnooks who fork out their hard earned cash for magical mangosteen juice? Too bad for them. Especially if they have diabetes, since the carb count on this juice whatever its putative "benefits" must be astronomical since it is mostly apple fruit juice concentrate and what little mangosteen juice it contains--very little I suspect, is very high in carbs.

BOTTOM LINE: The proprietary Mangosteen juice blend sold all over the internet will lighten only your wallet and improve the inflammation only of the egos of the dead enders who did this research.