Replies

• Thank you very much to Chris fir introducing the notions advanced by Adele Hite about the proper nomenclature of therapeutic carbohydrate reduction. It is a very powerful point to coin a terminology that is not only correct but offering a semantic bridge to many health professionals that do not make out the sense of what the word keto intends to convey. I would add, though, that given the fact that carbohydrate intolerance is so idiosyncratic and dependent on the quality and degree of insulin resistance, perhaps we should think about the terminology therapeutic carbohydrate calibration to incorporate the notion of individualized approach and the need to put in context nutrition, movement, sleep hygiene and de-prescribing of anti diabetic medication. Health practitioners diagnose and prescribe therapeutic carbohydrate reduction/restriction while other metabolic health practitioners support people in how to achieve results smoothly. I would also add that other than therapeutic interventions, there are individuals that seek carbohydrate restriction/reduction for general wellness aiming at healthy weight management, increased stamina, increased self-stem, and other wellness objectives which are not sharply focused on treating a health condition but rather oriented to better health and wellness. That audience may not identify readily with the notion of a therapeutic intervention. Metabolic calibration?
  May 22, 2021

• Yes I've shared the ACC/AHA guidelines with her. She also has a lot of physician friends and family members so she is well aware of the standard of care. It is despite all the encouragement by these physician friends that she is seeking recommendations on further risk stratifying. Appreciate your input, thanks!
  May 21, 2021

• A couple of thoughts. According to current ACC/AHA guidelines this patient is in significant need of a statin. If she's not been tried on numerous statins at varying dosages, she should be (if she will allow). As for non-statin therapy, this is a must. With LDL near 190 she has a very high likelihood of familial hypercholesterolemia. CAC or lipid NMR would not really add anything to your risk stratification given her LDL and glucose intolerance, especially if high-dose statin therapy ends up being taken off the table. As for glucose tolerance, you might just consider calculating a HOMA-IR with a fasting insulin and fasting glucose level.
  May 21, 2021

• well written, so true!
  May 19, 2021

• You're right, the numbers are essentially the same. Even the history of intolerance to a statin. I think you're suggestions to the PCP are all reasonable things to do, and things that I've considered and recommended. But if the CAC comes back non-zero, how hard would you push pharmacotherapy for primary prevention? I can imagine that I won't be too happy as a patient if my CAC came back > 0 and OGTT negative. Like other imaging results, I can't "unsee" calcifications in my coronaries, yet the only other option is taking a medication indefinitely that most likely won't prolong my life. Would it be better to not see the CAC, and not take a statin, if I know that I'm someone who wouldn't want to take a life-long medication? That's why I found it difficult to make a hard recommendation for getting a CAC. At the same time, given that most doctors love statins and there is a cut-off of LDLc 190 for statin tx regardless of calculated risk, I felt like I should give it more thought. And are you considering Zetia because she was intolerant to a statin? What about trying out a different statin, and at a lower dose? And finally, I've noticed that despite all the discussion around hyperlipidemia and pharmacotherapy, I don't see much discussion around the causes of elevated LDL in patients without co-morbid conditions (e.g hypothyroidism, CKD, etoh abuse, etc). Except for "genetics", which I think many times in adult medicine is a cop-out and discourages further inquiry. The data doesn't seem strong for dietary cholesterol being a major culprit. Would you happen to know of any other mechanisms? And thanks for sharing!
  May 17, 2021

• Cool article, thanks. I didn't know that Cochrane was going back and forth on this issue. Out of curiosity, would your risk assessment change for patients with confirmed FH or persistent LDL-c > 190? I agree that most women age < 50 and otherwise low risk may not benefit from a statin as much as many think. I think if this particular patient had an LDL-c around 140, for example, I wouldn't have gave it as much consideration. But because the LDL-c was close to 190, which is the cut-off provided by the ACC for when primary prevention with a statin is recommended regardless of risk, I thought I'd try to be more cautious. And to be honest, I have a bias toward less is more, especially when it comes to primary prevention of most things. My impulse is to defer statins for most people when used for primary prevention. I'm using this as a thought exercise so that I can provide a more nuanced discussion grounded in data when talking about it with patients, and other physicians. Thanks again!
  May 17, 2021

• Peter, keep in mind the known insulin-independent glucose uptake in myocytes that occurs after (and up to 24 hours after) resistance exercise.
  May 17, 2021

• I have an eerily similar case right now. Woman is 56 and non-Hispanic Caucasian but similar biometrics and markers: BMI 23, normotensive, HbA1c 5.6%, FBG 106 mg/dL, hsCRP 1.1 mg/dL, HDL 60 mg/dL, Trigs ~90 mg/dL, LDL ~200 mg/dL. Interestingly insulin 3.3 uIU/L. No known family history because adopted . This was at baseline, pre-keto, but she’s now been keto three weeks. As a PhD and MHP, it would not be responsible for me to counsel the patient alone, but I’ve suggested to her PCP a CAC/CTA, OGTT, lipoprotein, NMR, and Lp(a). Also a cGM. I’d be curious to know what your patient’s insulin runs, as I found it interesting that mine ran a low insulin (again pre-lowcarb) despite borderline HbA1c and high FBG. I’d expect elevation in the fasting insulin if the HbA1c 5.6% and high FBG was marking insulin resistance and am also encouraged by the HDL and trig levels. Lastly, the individual I described had previously tried a statin and was intolerant. Bad muscle cramps and fatigue. Depending on the CAC/CTA, NMR, and Lp(a) results, I’d like to have a discussion with her PCP about Zetia. It may not be necessary but it would be conservative. Caveat to all of this is my qualifications are as a PhD (ketogenic and neurometabolism) and MHP. I’m a rising medical student at Harvard with interest in this area and work as a nutritional consultant but absolutely am not qualified or capable to give patients medical directives and am careful in this respect. Still, you case intrigued me because it was so similar so I figured I’d share. Keep us posted
  May 10, 2021

• THERE IS A PANDEMIC OF OBESITY AND TYPE II DM, WHICH IS KILLING MORE THAN COVID AND CAUSING MOR MORBIDITY. IF THE GOVERNMENTS PUT AS MUCH EFFORT INTO EDUCATING THE MASSES ABOUT THE CAUSES (REFINED FOODS, SUGARS) WE WOULD SAVE MILLIONS OF $ AND LIVES AND THE HEALTH CARE SYSTEMS AROUND THE WORLD MAY SURVIVE.
  May 10, 2021

• Sharing widely! Young doctors giving me hope for the future of medicine!
  May 10, 2021