UNITY NOW! UNITY FOREVER! What Will It Take?

Definition of Unity from the online dictionary:

The state or quality of being one; singleness.

The state or quality of being in accord; harmony.

One of the best groups/communities I have seen in the past 4 years that really embodies UNITY is LIVESTRONG.  From what I have seen working with them for the past few years is there is little arguing about which type of cancer is worse. Doesn't matter whether it breast, colon, brain or any other type cancer is cancer and it is all bad.

Then we come to diabetes which has been my primary focus for the past 3 1/2 years. All there has been is arguing about which type is worse, type 1 or 2 or others, there are more. The arguing is so unneeded in this community where the disease is now a pandemic in the world. What is needed is unity not dissension.

About 2 1/2 months ago I left the diabetes community on Facebook and pretty much all over to take a break from the stress of what was going on and to take a look on the inside from the outside. What I saw bothered me. After 3 1/2 years it looked like all of our work and preaching hadn't done a thing. No one had changed their attitude about the types of diabetes and getting together to find a cure. Then a miracle happened just the other day.

Hang on though I want to cover one thing. A Cure. Everyone wants a cure for some disease. There are so many in the world we need cures now but there are so many obstacles. the thing is if we unite as friends and supporters for each other we can get to a point where we can demand answers, get answers and make things happen. Apart we are nothing, together we can and will win.

Back to diabetes and the lost communities, as I call them. Imagine with 360 million people in the world diagnosed and another 600 million walking around with diabetes, almost 1 billion people we are talking here, just imagine if we all came together to demand answers? Imagine if we all came together to demand a cure now? Imagine?

Anyway UNITY is important and I have had my say. Oh wait, about the miracle. Just recently I have seen to groups coming out of the closet and endorsing our philosophy of unity. I was amazed and shocked. Not that we received credit per se but seeing them write and post about coming together I knew our words and efforts have been heard. It was a great feeling to know people have been listening and maybe it took time but they are working on it. I am proud of everyone that is making the effort.

Thanks

Mark

Leave it Alone!

Hello all! It's been a while since I have posted on here but just wanted to quickly touch base on the Paula Deen (spelled it DEAN before. Sorry Paula and thank you Anna) stuff. stuff.

Leave the girl alone. I mean how many people out there don't talk about their diabetes? How many people are still in the closet? Why not let this lady do her thing?

To be honest a donut hamburger sounds great about now!

She has come up with some great recipes in her time for people who can eat these foods and there is nothing wrong with her catering to them. Those are her recipes and she can cook for who she wants too.

I heard the statement the other day "well she needed to tell us because we need to to speak for us." You know what I say. You don't need a celebrity to speak for us as diabetics, we just need ourselves. We just need to speak up and speak louder and that's it.

Be Well
Mark

Are Diabetes and Colorectal Cancer Risk Genetically Linked? Ali Torkamani, PhD

Type 2 Diabetes Risk Variants and Colorectal Cancer Risk: The Multiethnic Cohort and PAGE Studies

Cheng I, Caberto CP, Lum-Jones A, et al
Gut. 2011;60:1703-1711

Summary

Colorectal cancer and type 2 diabetes are common chronic diseases sharing a number of risk factors including age, diet, obesity, and physical inactivity. Studies have shown that individuals with diabetes have a 19%-30% increased risk of developing colorectal cancer,^[1,2] and this association between colorectal cancer and type 2 diabetes remains after adjusting for shared risk factors, suggesting that a core set of nonenvironmental risk factors may underlie their co-occurrence.^[3] Investigators from the Population Architecture using Genomics and Epidemiology (PAGE) initiative drew study subjects from the multiethnic cohort to determine whether shared genetic risk variants might explain this co-occurrence.

The multiethnic cohort consists of 215,000 individuals drawn from 5 racial/ethnic groups: African American, Native Hawaiian, Japanese, Latino, and White. Of these individuals, 2011 patients diagnosed with colorectal cancer and 6049 control subjects were selected for genotyping. Case subjects were identified through population surveillance covering Hawaii and California to capture incident colorectal cancers, and control subjects consisted of individuals between the ages of 45 and 75 years old with no diagnosis of colorectal cancer prior to enrollment. All of these individuals were genotyped at 19 single nucleotide polymorphisms (SNPs) previously associated with type 2 diabetes.

After statistical associations corrected for age, sex, and race/ethnicity were performed via logistic regression, 4 SNPs associated with type 2 diabetes -- THADA, JAZF1, KCNJ11, and TSPAN8 -- were found to be nominally associated with colorectal cancer risk.

Viewpoint

Although 4 type 2 diabetes susceptibility SNPs were associated with colorectal cancer in this study, there are a number of concerns regarding the accuracy of these results.

First, with the exception of the THADA SNP, the associations are quite weak, resulting in P values only slightly below the threshold for significance.

Second, with the exception of the KCNJ11 SNP, the directions of the effects for type 2 diabetes vs colorectal cancer were swapped. In other words, type 2 diabetes risk variants were associated with decreased risk for colorectal cancer in these SNPs, which is inconsistent with the original hypothesis that type 2 diabetes and colorectal cancer co-occurrence are mediated by common genetic mechanisms.

Third, a number of the considered populations are admixed, suggesting that correction for overall ethnicity may not be sufficient. Fourth, when analyses were stratified by type 2 diabetes diagnosis status, associations were observed among individuals with colorectal cancer but without type 2 diabetes, rather than those subjects with concurrent diagnoses. Finally, no replication or attempt to otherwise confirm the results was reported.

While there are a number of concerns regarding the accuracy of these results, the strong association for theTHADA SNP and the consistency of direction for the KCNJ11 SNP is intriguing. These associations also hold up, for the most part, when stratified by ethnicity, suggesting a true signal could be present at these loci. However, it is difficult to draw any solid conclusions regarding the relationship between type 2 diabetes susceptibility loci and colorectal cancer risk. Clearly, further studies need to be executed to clarify the genetic relationship between type 2 diabetes and colorectal cancer.

A Personal Approach to Cancer Care by MEDSCAPE TODAY

I'm John Maris, and I'm the Chief of the Division of Oncology at the Children’s Hospital in Philadelphia. Today I would like to talk to you about the concept of personalized medicine for cancer. There is a lot of press about this idea of personalized medicine. I would like to spend a minute defining how I think of personalized medicine and the remaining challenges related to this concept. I would like to highlight 2 of these challenges for you today.

In cancer, personalized medicine, to me at least, means being able to take the tumor specimen, the cancer specimen, at the time of diagnosis, and perform a series of assays that provides the clinician with a definable list of prognostic markers and therapeutic targets. The vision is that modern sequencing technology, proteomic technology, has the ability to determine all of the oncogenic vulnerabilities, or all the genes and pathways that are driving the tumor, identify those in a single or a limited number of assays, and provide an interpretable and actionable list of variables for the clinician.

A clinician takes variables to make a decision such as the stage of the disease or results of certain laboratories tests. [Personalized medicine] should add to that list and give the clinician a very precise way to administer therapy. We are on the cusp of this, as you know. There are assays available right now for use in individuals with adult and pediatric cancers where a genetic test influences the treatment decisions being made.

The promise is there. There is an enormous amount of scientific literature coming out on a weekly basis pushing us forward in this field and showing that this is not a pipedream any longer, but a reality, and it is coming.

There are many challenges. The first of these is that many of us in the field, and I must say that I was one of those, felt that the ability to read out every single base in our 3 billion-based comparison, to do a complete sequencing of a cancer genome would be the test that would need to be done, or that should be done, to provide all of the answers. What we have learned in the last several months is that that is naïve and not true. The idea that sequencing a cancer genome alone will provide enough information for the clinician is clearly misguided and not sufficient. Those of us in the basic science field need to integrate that sort of information with other information, such as gene expression, protein analyses, and other types of analyses. It is going to be a bit more complicated than many of us were hoping.

The second issue that is in the future but that we need to address now is the cost of this, how we are going to do this in a resource-limited environment, and how we can realize this promise without denying access to care to those who have less resources.

We cannot continue to use technology agnostic to the cost. All of us in this field have to think very carefully and clearly about what it is going to cost to implement these [advances] in the clinical setting. Those of us who are doing discovery work, biomarker and therapeutic arc of discovery work, have to work with many others in the field to come up with a realistic business plan for how these can be implemented in a way that is efficient.

In the big picture, implementing personalized medicine should save money because you are using more precise treatments, and a more rational strategy. There is going to be a transition period because these technologies are extraordinarily expensive. We are going to need to work together to figure out how to implement them.

A worst case scenario, for me, would be to develop techniques that are incredibly precise and have great ability to help patients, but to deny patients access because of the cost. This is something that we have to be very, very careful about in the next decade.

There is a tremendous amount of promise in a personalized approach to medicine in general and cancer treatments in particular. There is still a lot of work that needs to be done and we have to do this in a collegial and collaborative way with all aspects of the healthcare community to make sure that this is done in the right way.

Thank you very much for your attention.

Statins Associated With Significant Increase in Diabetes Risk from MEDSCAPE TODAY

January 9, 2012 (Boston, Massachusetts) — Statin use in postmenopausal women is associated with a significantly increased risk of diabetes mellitus, research shows [1]. New data from theWomen's Health Initiative (WHI) hints that the risk of diabetes is higher than suggested by previous studies, with investigators reporting a 48% increased risk of diabetes among the women taking the lipid-lowering medications.

"With this study, what we're seeing is that the risk of diabetes is particularly high in elderly women, and this risk is much larger than was observed in another previous meta-analysis," senior investigator Dr Yunsheng Ma (University of Massachusetts Medical School, Boston) told heartwire . "For doctors treating patients, we would like them to really look at the risk-benefit analysis, especially in different age groups, such as older women."

Annie Culver (Mayo Clinic, Rochester, MN), a pharmacist and lead investigator of the study, published online January 9, 2012 in the Archives of Internal Medicine, said that "close monitoring and an individualized risk-versus-benefit assessment is really a good thing, as well as an emphasis on continued lifestyle changes." Culver added that as the population ages, and because these patients have a higher vulnerability to diabetes anyway, monitoring for diabetes in statin-treated patients becomes more important.

"I think the risk [of diabetes] is definitely there for statins," Culver told heartwire , "and I think physicians are probably aware of this risk. I think we now need more information and more research about precisely how this risk translates to different people and different populations."

Previously Published Data on Statins and Diabetes Risk

Recently published data reported by heartwire highlighted the potential risk of diabetes with statin therapy. In June, Dr Kausik Ray (St George's University of London, UK) and colleagues published a meta-analysis of PROVE-IT, A to Z, TNT, IDEAL, and SEARCH--five trials testing high-dose statin therapy--and found a significant increase in risk of diabetes with higher doses of the lipid-lowering drugs. A meta-analysis published in the Lancet in 2010 by Dr Naveed Sattar (University of Glasgow, UK) also showed that statin therapy was associated with a 9% increased risk of diabetes.

In the present study, Culver, Ma, and colleagues analyzed data from the WHI, an analysis that included 153 840 postmenopausal women aged 50–79 years old. Information about statin use was obtained at enrollment and year three; the current analysis includes data up until 2005. At baseline, 7.0% of women were taking statins, with 30% of women taking simvastatin, 27% taking lovastatin, 22% taking pravastatin, 12.5% taking fluvastatin, and 8% taking atorvastatin. During the study period, 10 242 incident cases of diabetes were reported.

In an unadjusted risk model, statin use at baseline was associated with a 71% (95% CI 1.61–1.83) increased risk of diabetes. After adjusting for potential confounding variables, the risk of diabetes associated with statin therapy declined to 48% (95% CI 1.38–1.59). The association was observed for all types of statins.

"The association between diabetes risk and statin therapy was not observed with any one type of statin, and it seems to be a class effect," said Ma.

Subgroup Risk

A significantly increased risk of diabetes was observed in white, Hispanic, and Asian women (an increased risk of 49%, 57%, and 78%, respectively). Among African Americans, who made up 8.3% of the population studied, there was a nonsignificant 18% increased diabetes risk associated with statin use at baseline. Statin use and diabetes risk was also observed in women across a range of body mass indices (BMIs <25.0, 25.0–29.9, and>30.0 kg/m²). Women with the lowest BMI (<25.0 kg/m²), appeared to be at higher risk of diabetes compared with obese women, a finding the investigators speculate is related to phenotype or hormonal differences between the women.

In an editorial [2], Dr Kirsten Johansen (University of California, San Francisco), Editor of the Archives, noted that the increased risk of diabetes in women without CVD has "important implications for the balance of risk and benefit of statins in the setting of primary prevention in which previous meta-analyses show no benefit on all-cause mortality."

Ma agreed, noting to heartwire that statins are used with increasing frequency, including in primary prevention, and--based on the JUPITER trial--in patients with normal LDL cholesterol, but elevated C-reactive protein (>2.0 mg/L). In the present study, baseline statin therapy was associated with a significant 46% and 48% increased risk of diabetes in women with CVD and without CVD, respectively.

Just 7% of women in the WHI study were taking statins in the analysis, but today that number would be significantly higher, making the potential risk of diabetes at the population level much more widespread. Ma said that physicians need to evaluate the risk of diabetes as well as the potential benefits of statin therapy in elderly female patients, and start statins after lifestyle interventions have been attempted.

Better health, byte by byte

I found this article today through Google Alerts and with the work that we have done in the past and considered important, like environmental issues this just fit the bill for more food for thought.

I have always wondered the what if scenario of the cure. Are they looking for a cure based on something they know or don't know? Have they looked at the environment as a possibility? Have they looked at other forces of nature that could have been involved? Or are they juut looking at the boy and our medical life? 

These questions will most likely never be answered unless we stand together as one and ask them. Then again some readers will think I am nuts for even bringing this up. I remember a few years ago when we firat brought this topic to light and everyone looked the other way. Well here it is again so maybe I am not that far off?

We would love to hear your comments about this subject..

Thanks

Mark

Avoid Desiccated Thyroid Hormone Replacement

Desiccated thyroid hormone , Armour thyroid and Thyroid USP is listed as obsolete by the FDA but continues to be prescribed and used by some people . I recently saw a video promoting the use of desiccated thyroid which prompted me to write this note.

Our thyroid gland produces thyroid hormone in a response to TSH ( thyroid stimulating hormone ) from our pituitary gland. The primary form of thyroid hormone produced and released into our blood is T4 . This T4 is slowly converted to the active hormone T3 in our tissues,primarily the liver . The T3 Hormone in correct amounts helps keep all of the cells of our body running at peak efficiency.

A deficiency of T4 and T3 results in a slow down of all of the machinery in our body and an excess of T4 and T3 can have toxic effects especially for our heart causing arrhythmia , heart failure , angina or even cardiac arrest. The effect of excess T3 is a concern for anyone with heart disease.

( many of us have a little silent coronary heart disease ).

So, why is desiccated thyroid hormone not a recommended treatment for hypothyroidism ?

Desiccated Thyroid Hormone is of animal thyroid tissue origin. This means that it contains a mixture of T4 and T3. The T3 is almost 100% absorbed rapidly producing abnormally high levels of T3 in the blood stream and potentially a toxic effect on that persons heart.

Levothyroxine ( L-thyroxine , levothyroid , synthyroid and others) is T4 and is much safer to use. The T4 is absorbed and converted slowly to the active T3 , similar to the function of a normal thyroid gland. Be safe . If you need thyroid hormone replacement, use T4.

Dr. Calder