My particular question is about Nicotine-Derived Nitrosamine Ketone (NNK) and whether NNK accelerates the production of βHB in the fat adapted individual much like other exogenous ketones?
Since I have quit chewing tobacco 9 weeks ago I have gained 12 pounds of adipose. My βHB averages are lower. It was 1.3, now I am .3. BG has gone up as well from an average of 4.9 to 5.5. In efforts to limit this effect I moved to lower and lower carb averaging 0-10 g a day. And now I am back to square one trying to understand my new ketone and glucose levels since nicotine cessation. If possible I would like to hack how my body is responding to the lack of nicotine.
Background Information Nicotine and Insulin Resistance:
After Ketofest 2018 I promptly came home and quit chewing tobacco because I too wanted my health story to be the best one I could tell. I met so many inspiring people and I knew I could continue my health journey by quitting tobacco and so I did. I immediately struggled with weight gain going from 17% BF to 22% BF with a 12 pound increase of adipose using a Dexascan before and after. I reached out to @richard who was not familiar with the effects of nicotine. No problem, let’s go find the science I told myself!!
Since then I have found that nicotine has an acutely positive effect on lipolysis through multiple mechanisms. Adipose itself remains insulin sensitive even as the muscle and other cells becomes insulin resistant. This means nicotine helps us use our fat stores. This is something that has been know since at least 1928 when Lucky Strike cigarettes marketed themselves as preventing a weight gain (see photos). Nicotine creates a preponderance of free fatty acids while acutely increasing mTor. This increased FFA through the hepatic function allowed for utilization of fats. It seemed that insulin could be ignored to some extent under the influence of nicotine!!! AND MY personal use was one tin a day or the equivalent of 4 PACKS of cigarettes!! So I was impacting my lipolysis heavily.
Stopping Nicotine does this:
- On average a 10-15 pound weight gain.
- A 3 fold chance of developing T2DM within 2 years up to 12 years.
- An increase in insulin resistance measured by a HOMA-IR scale.
- IRS-1 Ser636 phosphorylation DECREASED significantly in nicotine cessation.
( Bergman BC, Perreault L, Hunerdosse DM, Koehler MC, Samek AM, Eckel RH
. Intramuscular lipid metabolism in the insulin resistance of smoking. Diabetes 2009; 58 :2220–2227pmid:19581421)
The only way to reverse this insulin resistance was to take rapamycin which is not a good thing to do. This drug was invented to decrease chance of tissue rejection and helps inhibit the mTor and not to hack lack of nicotine…sigh.
I have decided it is better to be done with chewing tobacco and to have gained back some weight than be more slender and risking mouth cancers. Still it is discouraging. Since the beginning of September I have gone back to basic keto, no fasting and no timed meals in an effort to reclaim my previous βHB averages. This past week I once again started to get 1.2 βHB mmol and this morning got my first 4.9 in over 60 days!! Next week I plan a 5 day fast and following that either 18/6 or 3 X 36 hour fasts to help shut down mTor.
Any other suggestions based on how nicotine interacts or past experience is welcome!!