LOST KETOSIS

(Michael Dowd) #1

Hello, newbie to this forum.

Some background first. Four or five years ago I went on a ketosis diet and was successful in losing about 45 pounds and continued to maintain that weight and eat a ketogenic diet with lots of healthy fats keeping NET carbs around 20 to 30 grams a day. I felt great and was an active person. This spring a cardiologist told me I had afib and put me on the blood thinning drug Eliquis. Since that time I have maintained same diet every week but have now put on 15 pounds.

Presently I am a loss to understand what is going on with my body. My KetoSens monitor gives me readings of .4 to .7 for the last 2 weeks (which is below and barely into ketosis). I have kept my carbs under 20 “TOTAL” carbs a day. I record everything I eat in a spreadsheet which generally shows that my grams of fat being almost twice as much as protein and my caloric intake averages 1500 to 1700 a day. Again I like to walk/hike and am reasonably active.

I just turned 80 but most everyone tells me I am in remarkable condition for my age.

I would appreciate an insight into what might have happened on my Keto journey.

(Robin) #2

Welcome!
Do you feel the weight you gained is truly overweight? I’m 70 and had lost too much weight on keto. So I tweaked some things and ate more calories, but remained keto. I slowly gained weight back to a healthier range.
I have heard that older folks need some “reserve” with weight. But I don’t know if that’s true.

(Bob M) #3

Whenever you take a drug, you have no idea what will happen, because these are barely tested on anyone, let alone a group of people who are keto.

For ketones, unless you feel better getting higher ketones, I wouldn’t worry about it. Mine are usually 0.2 mmol/l in the morning. When they came up with the idea of “ketosis”, everything was new, and they really didn’t have a lot of references.

It’s also relatively easy to get to high levels when you start, but it seems harder the longer you’re producing ketones. But it’s also highly individual. Listened to a podcast where they were discussing a keto diet for cancer, and they said that two people eating the same diet can have vastly different ketone levels.

If you feel good, then I wouldn’t worry about the ketone levels. If you feel better at higher ketone levels, that’s a different story.

(Joey) #4

So true for most of us who’ve been through this … but to put a finer point on this, I believe it’s common to see higher ketone levels initially because your body is producing far more than can be efficiently used (while your mitochondria are transitioning).

Over time, when you’re “fat adapted” (ketone-adapted is likely more accurate description), your body produces less (i.e., sparingly; no more than can be used) and your tissues are using more (they’re adapted to this alternative energy source). Hence, your measured serum/urine/breath ketone levels are lower.

One additional thought: As more and more serious researchers are coming to believe, when your blood is circulating ketones to fuel your body’s tissues, your LDL cholesterol increases. That’s neither dangerous nor unhealthy. It’s what cholesterol is for!

:vulcan_salute:

(Bob M) #5

I think you’re right/correct. I also think this “keto adaptation” is like the physics theory that a moving body stays moving: it’s hard to “lose” keto adaptation. Even eating a bunch of carbs, I don’t think you lose ketone adaptation (though you may not register any BHB for a while). You drop the carbs, go keto again, and your back into low ketones. (Now, how long your carb binge can be, that I can’t guess. I’m assuming a few days to a week won’t hurt, but I don’t know.)

(Megan) #6

Hi, welcome to the forum. Ask your cardiologist if there is a different drug you can try. Maybe one that uses a different mechanism to thin your blood, or maybe a lower dose of the one your currently take. Also ask if you have any other risk factors, apart from your age, for having a stroke.

You are very definitely in ketosis with readings of 0.4-0.7. Is there a reason you want your readings to be a lot higher? Apart from the effects from the weight gain, do you feel less well and active at the moment, compared to when your blood ketones were higher?

Keep us posted and welcome again.

#7

Weight gain is a known side effect of Eliquis, seems to be more prevalent in women, I’ll make a leap of a guess that prior they never checked cholesterol breakdown, actually scanned you to see if you had arterial plaque, or any actual risk factors of clotting, if not, I’d question why you’re on it to begin with. AFIB is a heart rate issue, not a thick blood issue, doesn’t mean you don’t have that, but simply having AFIB doesn’t mean your blood is thick and at risk for clotting either. Doc’s like the throw people on things they don’t need when it comes to heart stuff regardless of whether they need them or not. Beta Blockers (may) make sense to control racing heart rate, but unless you actually display a risk factor for clotting, turning your blood into water and the downsides associate with it aren’t justified.

No such thing, you’re either in Ketosis or you’re not, having ketones in your blood is all it takes, ketone levels had nothing to do with fat loss speed. The only time that number ever matters is for epileptics or if you’re trying to treat a medical condition that directly requires high ketone levels to accomplish. Useless for fat loss though.

Total vs Net is also not really a concern, the reason we net our fiber and sugar alcohols is because you’re not processing them, those carbs aren’t carbs to us because humans don’t make the enzyme required to digest them, our guy bacteria does use them, and that’s helpful for digestive health. Make sure you’re getting plenty of protein, for most people fat intakes, even on keto, half of that in protein is most likely a deficient amount, especially being physically active. Losing muscle and bone mass is the absolute last thing you need at 80. I don’t need to tell you the saying break a hip die of pneumonia, most people don’t break hips (or any bones) from simple falls when their hips aren’t paper thin from long term low protein diets. Being active and hiking is a great way to (not) have that happen on either the muscle or bone mass benefits, but won’t matter if you don’t have the protein to build it all, and fat won’t.

(Michael Dowd) #8

Thanks everyone, very interesting. I think I paid too much attention to the fact that my blood ketones frequently were less than 0.5mmol/L for much of the time (online info said not in ketosis) and being baffled by the weight gain.

I suspect that the drug Eliquis has had an effect on my body chemistry or my metabolism. As I said I had been eating the exact same weekly Keto diet for years when all of a sudden I started to put on weight the same time as starting Eliquis. I think too that Bob M is correct in that you really don’t know the effects of any drug.

While I hate trying to keep TOTAL carbs at less than 20 grams a day, at least I don’t get hungry at that level and I am hoping to get back to a good weight and feel better too.

(Alec) #9

Pinging @FrankoBear

FB, you had/have afib didn’t you? Are you taking that drug (or similar)? Any similar experience here or words of wisdom?

(Joey) #10

I’d imagine that, at some point, with ample carbs ingested again, one’s mitochondria re-adapt away from ketones back to glucose. How long? Who knows … but perhaps about as long as it took that same individual to become “fat adapted”? :man_shrugging:

(You've tried everything else; why not try bacon?) #11

Both Dr. Stephen Phinney and Prof. Jeff Volek, who defined the term “nutritional ketosis,” have said that the 0.5 reading is somewhat arbitrary. It’s just the level at which they felt they began to see benefits of the ketogenic way of eating.

The real point of the diet, in my opinion, is to lower glucose intake and lower serum insulin. The presence of ketones is an easily-measured effect of the lowered insulin and glucose. (Note that there is at present no way to measure serum insulin, except by means of a laboratory test.) And the fat loss that often accompanies the diet is a much-prized side-effect, because so many of us got fat eating a high-carbohydrate, low-fat diet.

So my question would be what the Eliquis is doing to your serum glucose and your serum insulin. Even if all the weight you are gaining is from storing fat, it still might not be a problem where your metabolic health is concerned. Dr. Robert Lustig makes this point: about 20% of the obese are pefectly healthy, just overweight. It was for them that the medical term “metabolically healthy obese” was coined. The converse is the significant percentage of lean people with metabolic disease, described as “thin on the outside, fat on the inside”: (TOFI) in the medical literature. And there are actually more TOFI’s out there than MHO’s. .

Granted, if you are eating a ketogenic diet solely to shed excess fat, seeing the number on the scale go up, even when it’s from additional muscle, not from additional fat, can be grounds for freaking out. And if it’s a medication that is supposed to be helping you, it is normal to feel betrayed. Perhaps there is a different anti-coagulant that you might take, that wouldn’t make you fatter?

Of course, all drugs have potential risks and benefits. My mother’s cardiologist and I had a number of go-rounds about her Eliquis prescription. The doctor was quite frank that from his point of view, it was a tough choice: whether to let the patient die of a heart attack, or to prescribe a drug that would prevent the heart attack by killing the patient from a brain haemorrhage instead. Either way, he was risking a lawsuit. We never did decide what to do, before Mom had a fatal fall instead. And for the record, I would never have sued him for doing his best, no matter the outcome.

(You've tried everything else; why not try bacon?) #12

FIFY!

And seriously, it is a matter of damage, not adaptation in one direction or the other. Damage to the mitochondria is the very definition of metabolic dysfunction, in my book.

(KM) #13

Throwing a slightly unrelated spanner in the works … Is there really scientific evidence of keto / fat “adaptation”? I always wondered if it wasn’t just keto flu, really a lack of needed salt, making people think there was some required transition period. To me it seems extremely strange that the body wouldn’t “know how to use ketones” or fat. It’s a chemical reaction, not an algebra equation. If there is really a transition period, could it possibly be a transition of gut bacteria species that has to take place when one fuel is subbed in for another???

(Joey) #14

Hmmm…

Excess glucose in circulation produces insulin release overages which in turn cause significant system-wide tissue damage. But I didn’t know that glucose damages the mitochondria … are you sure?

#15

Of course the body knows how to use ketones right away but fat adaptation is still a thing. Many of us very clearly notice when that happens. Active people notices differences too regarding their performance.
I even heard that there is the basic fat adaptation (I got that after 7 weeks) and something later (I lost my water weight changes at some point, it seems it doesn’t happen to everyone).
After short carby times nothing happened but when I strayed for too long, I started to feel like before fat adaptation… And I ate much carbs this summer compared to my normal, probably last year too and I have water weight changes again… But maybe not because of that. I have no idea what my body does with my glycogen stores…

(You've tried everything else; why not try bacon?) #16

According to Phinney and Volek, yes, there is research, and plenty of it.

  1. As I keep repeating all over these forums, fat/keto-adaptation is a specific process that involves the healing of mitochondria in skeletal muscles and the reactivation of certain fat-related metabolic pathways in those same muscles. It is generally a six-to-eight-week process, though a few people can accomplish the healing in a shorter time and a few take much longer. This healing process is unavoidable, and endurance athletes notice a distinct decrease in their performance during this time. This is why we always advise going easy on the exercise during fat-adaptation. These same athletes also report that, once the re-adaptation is complete,their performance returns to pre-keto levels, and in many cases exceeds them.

  2. As I also keep repeating all over these forums, the “keto flu,” on the other hand, is completely preventable, because all it is is a lack of enough sodium in the body. One of the many effects of hyperinsulinaemia is to slow the excretion of salt by the kidneys. When we cut our carb intake sufficiently, our serum glucose drops, and therefore our serum insulin drops. This takes only around 24 hours. The result of the normalisation of serum insulin is that the kidneys quite naturally return to their normal level of sodium excretion, so we start needing more salt in our diet than we have become accustomed to. Couple that with the fear of salt that has been instilled in us along with our love for carbohydrates, and you can see that there might be effects from not getting enough sodium.

It so happened that I watched a video lecture by Dr. Phinney before going keto, in which he happened to mention all this, and thus, forewarned, I never experienced the “keto flu” because I made sure to put enough salt on my food.

I hope that clears it all up for you.

(You've tried everything else; why not try bacon?) #17

Yes. It’s a lot less damaging than fructose, ethanol, and the branched-chain amino acids, so the effect is much slower. But the mitochondria are specialised for metabolising fat, and while they can handle glucose, the reactive oxygen species produced in glycolysis, together with the advanced glycation end-products it produces, damage the mitochondria. By contrast, fatty-acid metabolism produces very few (if any) reactive oxygen species, and no advanced glycation end-products.

The foregoing is in spite of what I posted earlier about glycolysis being an evolutionarily ancient process. Remember that the mitochondria have been able to shed most of their original DNA in order to specialise in fatty-acid metabolism. I would expect that point to be relevant here.

Remember, too, that glucose also damages the red blood corpuscles, even though they require glucose in order to live. The body has evolved a means of handling this, and the red blood corpuscles only live for around ninety days anyway. Apparently our ancestors failed to eat enough carbohydrate to evolve (or to avoid losing) the ability to repair mitochondria in the presence of glucose in quantity.

(Megan) #18

The risk of forming blood clots comes from afib stopping the blood from moving through the heart normally. It can pool in eddies and move more slowly in response to the way the muscles are contracting.

In saying that, I’d be wanting a lot more info and testing before taking this drug @MJD142 Michael.

(Joey) #19

I recall Dr Thomas Seyfried has experimentally shown that damaged mitochondria are the underlying cause of tumor propagation once a cancer begins - and that there are several common causes of such mitochondrial damage. But I didn’t recall elevated serum glucose levels to be one of them.

I seem to recall he demonstrated that serum glucose feeds tumor propagation once it is underway - not as the cause of the mitochondrial damage itself.

I’ll have to go back and re-read some of his papers (and excellent book on the topic) and refresh my understanding. Thanks.

(You've tried everything else; why not try bacon?) #20

I imagine the good doctor was concentrating on more immediately mito-toxic substances.

Also worth mentioning is that I understand his position to be that mitochondrial damage, whatever the cause, is the cause of all cancer. He and others have done experiments with cell nuclear transplants, and nuclei with damaged DNA put into cells with healthy mitochondria do not result in cancerous cells. However, the reverse–undamaged nuclei put into cells with damaged mitochondria will become or remain cancerous. So it is clearly the miochondria, not the nuclear DNA, that is the determining factor.

The reason for the Warbug effect, as I understand it, is precisely because of the mitochondrial damage. The cell can no longer metabolise fatty acids or ketones and must rely on fermentation and glucose as its energy sources. (Those reactions can take place anywhere in the cell; there is no specific organelle involved.) The unrestrained growth typical of cancer is a downstream effect of the mitochondrial damage since, among other reasons, healthy mitochondria are essential for regulating cell apoptosis.

All that said, it must also be borne in mind that a high-carbohydrate diet is well-known to associate with much higher cancer rates. Nina Teicholz says that the FDA and the NIH were so alarmed by the data that they convened a special conference to decide what to do. In the end, it was decided that a high-carbohydrate, low-fat diet was so important to cardiovascular health that the public should not be “confused” by adding a cavet about cancer to the public message.