A recent paper claimed that nonalcoholic fatty liver disease is an unrecognized epidemic. There is no FDA approved drug for treating and reversing NAFLD, however, sustained weight loss can reduce the risk of cardiovascular events and diabetes. Unfortunately, the article did not address how to be successful with weight loss. Weight loss attempts have obviously been unsuccessful if NAFLD is now epidemic. “Both NAFLD and CAD represent end-organ manifestations of the same systemic metabolic insult, all related to insulin resistance.” What the authors did not address is that the cause of the insulin resistance is hyperinsulinemia, and not the other way around. (Thank you, Jason Fung, for introducing this concept). In my last newsletter I described the lack of success and the increase in harm we have recently encountered with commonly prescribed diabetic medicines. Not only are we not making a dent in CVD prevention, but we now see an epidemic of NAFLD as over 70% of diabetics have NAFLD, which apparently is not being controlled by standard diabetes treatments. And I wouldn’t expect it to as I now have an understanding that diabetic meds don’t get rid of serum glucose, rather they drive the glucose into another compartment: the cell. I believe that this increase in NAFLD is due to our inability to understand the mechanism of current medicines which increase production of, or function of, insulin that drives glucose into the cells. Overloading the cell with glucose is not the solution. Rather, preventing intake of glucose by diet, maintaining a fasting state to provide ketosis to reduce visceral and intra-organ fat, preventing storage of glucose into glycogen and fat, increasing metabolism of fat, and increasing excretion of glucose, as opposed to sweeping it under the carpet or into the cell, is the solution. And the basic underlying problem is hyperalimentation of glucose and sugars that result in hyperinsulinemia when the cell cannot handle the increased glucose load caused by the hyperalimentation.
Professor Samuel Klein states that 2 million people have cirrhosis caused by NAFLD. However, the main cause of death is not liver failure but is CVD and the incidence of CVD continues to increase despite multiple drugs used to prevent DM and CVD. It’s the hyperinsulinemia that increases fat deposition in the liver and adipose tissue. Weight loss reduces visceral and liver fat, but this is difficult to implement. Well, not if you know how to do it. Jason Fung and his staff will take us through the educational process to understand how to be successful in treating ourselves and our patients. Nevertheless, not everyone can be successful as our hypothalamic set point fights us by slowing down our metabolism to maintain a set weight and body mass index, which can be difficult to overcome. I too will demonstrate my success with patients in helping them maintain optimal metabolism, which maintains weight loss. I will also provide all the literature support and studies demonstrating safety and efficacy of optimizing hormones, but probably different to what others are accustomed to doing. I will also provide all the studies that practitioners should be familiar with when optimizing HRT. Our focus should be on prevention, treatment, and reversal of disease which has not occurred in the majority of trials for CVD prevention using conventional medications.
The following are excerpts from recent papers from JAMA and NEJM:
“However, a resurgence of diabetes complications has appeared in national statistics and in the epidemiology literature. An increase in diabetes-related amputations has occurred nationally. Updated national statistics indicate that the recent increase in complication rates is occurring in middle-aged adults, among whom the risk of hyperglycemic crisis, AMI, CVA, and amputations each increased by more than 25%.” We obviously are not doing something right. “Most counties in the U.S. have seen an increase in cardiovascular disease mortality among adults.” Hmmm, just what is it that we are doing wrong that’s not working? Rather, what should we be adding that we are not? Perhaps not giving drugs that drive glucose into the cell should be a start. Other than type I diabetes, I know of no other disease entity in which there is a deficiency of glucose entering the cell. If the cell is storing glucose as fat, triglycerides, and glycogen, then the cell is already overloaded and getting plenty of glucose on its own. If the liver, kidney, pancreas, and visceral organs are all storing excess glucose as fat, then there is plenty of glucose getting into the cells. Enter diet, exercise and life-style change. Secondly, we should be disposing of the glucose by every other means possible and keep it out of the cell. Next we should be preventing the glucose from getting into the cell by metabolizing it in muscle and liver. Enter hormones. Next we should be providing less glucose into the body in the first place. Enter Jason Fung. (I’m currently fasting as I write this, and it really is easy.). Lastly, we should be disposing of and excreting the glucose that enters the body. Enter the new diabetic drugs. Perhaps we should be preventing this metabolic insult instead of just treating the disease by pushing serum glucose into the cells. That has been Dana’s goal for 20 years-establishing a medical academy that focuses on health and wellness, and promotion of that concept to physicians. This next Hormones and Beyond Cardio-Metabolic Symposium brings all this to fruition. Other medical academies attempt to reach this goal but have failed. And that’s why I am so excited about the upcoming Hormones and Beyond Symposium.
“This means that the future direction of diabetes complications has enormous collective implications for health and costs.” (JAMA 2019;321(19):1867-68). Yes, but why do studies show that CVD and outcomes are getting worse? And why is it that spending billions of dollars on health care and medications do not result in less CVD? Here’s why as explained in JAMA.
“Optimal diabetes care is predicated on balancing the immediate and long-term sequelae of the disease and its therapies and improving patient health and well-being. Professional societies have focused on HgBA1C levels to gauge the quality of diabetes care. The preferential use of HgBA1C levels in research, policy, and practice stems from the demonstrated association between lower HgBA1C levels and disease endpoints. (Observation does not prove causation and a correlate does not a surrogate make). However, these studies did not demonstrate improvements in outcomes that are most meaningful to patients such as CVD, stroke, and mortality. Thus, HgBA1C level is a surrogate marker for a proxy of uncontrolled disease. (Remember, just because high levels portend harm does not mean that lowering HgBA1C fixes the problem. And that depends on how one lowers the HgBA1C by either driving glucose into the cell ((bad)) or metabolizing it ((good))).”
“Similarly, for clinicians, HgBA1C level is an effective monitoring tool that is responsive to real-time changes in blood sugar control. Nevertheless, even though HgBA1C level is a valuable forewarning of future events in patients with diabetes and has an important role in reflecting the patient’s average level of glycemia, it (HgBA1C) should not be the outcome that matters most or that is prioritized at the expense of meaningful outcomes that are important to patients (and us).”
“Fallacy of the Surrogate: The rationale for using HgBA1C level as a surrogate marker for diabetes outcomes is predicated on the assumption of its direct correlation with improved outcomes that patients and doctors value like MI, CVA, and quality of life. Yet, the strength of this relationship has been called into question as the outcomes can be worse (even though the HgBA1C is lower). Meta-analyses revealed a null association between intensive glycemic control and these cardiovascular outcomes.”
“However, the importance of glycemic control for patients with type II diabetes cannot be extrapolated from data developed among patients with type 1 diabetes. The glucose-centric model of type 1 diabetes cannot be transferrable to the management of type II diabetes.” (In type I DM there is a deficiency of insulin and intracellular glucose whereas in type II there is excess insulin and intracellular glucose). Moreover, HgBA1C level may be misleading and its singular prioritization could lead to patient harm.” Yikes!
“The new GLP-1 RA and SGLT-2 inhibitors were demonstrated to reduce major macrovascular events and death independent of glycemic control.” (In other words, these new meds can lower CVD disease by other mechanisms other than lowering serum glucose). Then, what parameters and outcomes should we measure and follow? “Consideration should be given to reverse the routine use of surrogate markers like HgBA1C and instead refocus on the following outcomes that are important: CVD. Encouraging clinicians to embrace patient centered care unencumbered by the constraints of the HgBA1C level could allow them to instead focus on the outcomes like CVD. To improve the quality of value of diabetes care, it will be necessary for patients and all those involved in their care to focus on what truly matters-that which improves their lives and outcomes, and not their laboratory numbers.” (JAMA 2019;321(9):1865-67). Bingo!
I hope that the foregoing was as enlightening for you as it was for us. I’ve stopped chasing HgBA1C levels and the fruitless administration of expensive diabetic meds that lower HgBA1C but not disease outcomes. I now focus on lowering HgBA1C levels by other means. Instead I chase waist circumference, visceral fat, body weight and BMI, vascular responses, lipid levels, plaque scores, quality of life, and patient satisfaction. That’s what Hormones and Beyond is all about. Hope to see you in Austin.
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