Type 2 Nutrition #408: Keto-adapted vs. Fat-adapted

If you eat Very Low Carb (VLC) – not just low carb – you undoubtedly will know the term keto-adapted. There’s no formal definition of VLC because it varies according to your metabolism – the degree of your dysregulated glucose metabolism due to your degree of Insulin Resistance. However, VLC is generally meant to be a dietary intake of less than 50 carb grams a day. For many is means less than 30 grams; for me it is just 15 grams a day.

When someone eats VLC, they generally eat less food because 1) fat is filling and does not induce the pancreas to secrete insulin,  2) protein digests slowly and make you feel full longer, and 3) carbs are digested quickly and they make your blood sugar rise and fall quickly and thus makes you “hungrier, quicker and oftener.” And, if you eat VLC, when your body has used up the energy from the carbs you ate (and some that you have stored in the liver), your body has to turn to fat for energy – the fat you ate and then fat that is stored on your body.

Protein isn’t used for energy directly. It components, amino acids, have myriad other functions in the body; however, most amino acids can be used to make glucose in a pinch or, in type 2 diabetics, even when not needed. That’s one of the reasons type 2s take Metformin, to suppress this unwanted glucose production.

So, generally then, when a fat cell (a triglyceride) is catabolized (broken down) into its parts, you get 3 fatty acid molecules and 1 glycerol backbone molecule. A ketone body is a byproduct of this fat cell breakdown and oxidation. It’s a normal process. Repeating then: Being keto-adapted means that your body is making ketone bodies as part of this normal process where it is breaking down body fat (or dietary fat) for energy.

When eating a VLC Ketogenic Diet (VLCKD), blood ketone concentrations are generally above the 0.5mmol/L level. When they are from 1.5mmol to 3.0mmmol/L, they are optimal. Eating in such a way as to achieve this level of ketone bodies in your blood is healthy. It is, in fact, the normal metabolic state when fasting…as when we eat just one meal a day or one meal every three or four days, the way our hunter/gatherer forebears did.

My recent personal experience with extended 2 and 3 consecutive day fasting supports this view. Many others report similar outcomes. My metabolism has not slowed down. I am fully energized. When I eat VLC on “feasting” days, I know that my body is fully fueled by stored fat while “fasting.” It can do this because, when consistently eating VLC, the body’s blood insulin levels drop, allowing access to body fat (and ketones) for fuel.

The state of being in ketosis – this normal state – is not the same as having a condition called ketoacidosis. As the name implies, ketoacidosis is a diseased state, a serious form of acidosis. With ketoacidosis, the blood concentration of ketones is generally 20-30mmol/L, a full order of magnitude, i.e. 10x, higher. Ketoacidosis is a life-threatening condition and requires immediate treatment and hospitalization. I point this out because some current pharmaceutical advertising inexplicably uses the term “ketoacidosis” as though it were a condition that you could be walking around with. Acidosis is a serious, acute, unrelated medical condition.

Ketosis, on the other hand, while a normal state, is NOT a necessary state to be in in order to be a fat-burner. I have in past somewhat carelessly used the term “keto-adapted.” I do not own nor have I ever used a meter to test ketones. I test my blood for glucose, not ketones. Neither have I ever used keto strips to test my urine.

I have just assumed that I was in ketosis when I ate as few as 15 or 20 or 30 carbs grams a day, and certainly when I was full-day fasting (300kcal/day including only about 5 carb grams). If you are eating VLC (and fewer total calories), and your metabolism is operating at full energy, you are burning FAT for energy. You are fat-adapted, whatever you level of blood ketones. And that is your object: When fasting – as when between widely separated meals – to burn body fat WHILE YOU CONTINUE TO OPERATE AT FULL ENERGY LEVELS. Nature built us this way, to be in “nutritional ketosis.” Otherwise we would have become extinct long ago.

Type 2 Nutrition #407: Am I non-diabetic now?

Am I non-diabetic now? Seriously. Apparently there’s some disagreement about this. As I said in Type 2 Nutrition #439, a clinician told me that, 31 years after I was diagnosed (later with an 8.9% A1c), and after 15 years of eating Very Low Carb (VLC), with a 5.2% A1c now, I am no longer diabetic. I disagreed. I said that though my Insulin Sensitivity has improved, I am still Insulin Resistant and therefore Carbohydrate Intolerant. I said that I keep my Type 2 Diabetes in remission by restricting carbohydrates (VLC with Intermittent Fasting).

Then, a few weeks ago Megan Ramos, the Director of Jason Fung’s Intensive Dietary Management program, in an emotional rant on Facebook, said that “there are a lot of ‘haters’ out there” who say that, with an A1c of ≈4.5%, she is “not really non-diabetic anymore”; “[She’s] just controlling [her] diabetes with diet.” “Haters”? Huh? Well, isn’t that how she is controlling her diabetes?  Or does she think she is “cured”? In my case, I know that I am NOT cured. If I ate a lot of carbs again, my A1c would skyrocket!!! My guess is that hers would too, regardless of the fact that she doesn’t want to and never will eat that way again (i.e., “pasta 5 nights a week”).

Apparently, people who tell her that she is “just controlling her diabetes with diet” have hit a raw nerve…so I won’t tell her, but I am not a “hater.” I just prefer to look at my condition as one that I need to manage. And it is difficult to manage a condition if I am in denial that I have it. But, I’m willing to take a fresh look at the subject. Am I “non-diabetic” if a doctor who takes my blood (and doesn’t take a history) sees that my A1c is 5.2%? (In my case, besides my Way of Eating, I am also taking 1500mg of Metformin to suppress unwanted glucose production and improve insulin sensitivity, but this does NOT account for my “non-diabetic” A1c.)

So, with respect to my own condition, the matter comes down to whether I take a physiological or a psychological view. I cannot speak to Megan’s approach, nor can I address it from a medical POV; I am not a doctor. Neither am I an insurance underwriter who might take into account my history in setting a life insurance premium. Is it possible, from a life insurance underwriter’s POV, to at one time have been a diagnosed type 2 and then, later in life, to no longer be a diagnosed type 2 diabetic?

Age at onset of diabetes is doubtless a factor too. Incipient type 2 diabetes is undoubtedly more treatable and less intractable at an early age as less beta cell function has been lost. Megan notes that she was diagnosed at age 27 and fortunately found the right treatment immediately. Under Dr. Fung’s direction, she began to eat VLC and incorporated fasting from the get go. In 6 months, she lost 60 pounds and her A1c dropped to 4.5%. Today at 33, Megan takes no diabetic meds that I am aware of, eats LCHF and with fasting is 80 pounds lighter.

I was diagnosed at age 45 but continued to eat a Standard American Diet (neither my doctor nor I knew any better) for the next 16 years. I continued to gain weight and my type 2 diabetes got “worser and worser.” In 2002 I was maxed out on a sulfonylurea (Glyburide) and Metformin and starting on Avandia, a TZD. I weighed 375 pounds. Then, my doctor read Gary Taubes’s “What If It's All Been a Big Fat Lie,” in the New York Times Sunday Magazine (July 7, 2002) and suggested I try the diet described (20g of carbs a day) to lose weight!!!.

Today, 15 years later, thanks largely to eating Very Low Carb, I weigh 190. A little over a year ago, thanks to a suggestion from Megan Ramos, I began full-day fasting. I started with alternate day, then 2-consecutive day and now 3-day 300kcal fasts almost every week. I maintain my 185 pound weight loss by accepting that I have intractable Insulin Resistance and will therefore be Carbohydrate Intolerant for life. As such, while I am now clinically “non-diabetic,” and like Megan intend to stay that way for life, I know that if I ate the way I did before, I would quickly be a “clinical type 2 diabetic” again. Therefore, as a realist I have to say my type 2 diabetes is NOT cured; instead, my type 2 diabetes is IN REMISSION, and that “I control my diabetes with diet.” I will live happily and healthily and hope to remain that way for so long as I accept that reality.

Type 2 Nutrition #406: Triglycerides and LDL-C while eating Very Low Carb

Michael Eades, MD, somehow has me on an “early notice” email distribution of his blog. He and his wife, Mary Dan (MD), also an MD, are early backers of the LCHF Way of Eating and authors of “Protein Power” (1996), and “Protein Power Lifeplan” (2000), and many other books. He blogs at www.proteinpower.com/drmike. A recent post was titled, “How to Lower Your Cholesterol, using diet to keep your doctor off your back.”

I had a question about a screen shot of his lab LDL-C so I emailed him, and he explained that it was not “Calculated” by the Friedewald equation but was “Direct.” (The report actually said that; I just missed it.) He then provided me with a link to a post he wrote a few years ago, Low carbohydrate diets increase LDL: debunking the myth. This is another post about the effect of Low Carb diets on TGLs and LDL-C. You’ll need to read to the end of Dr. Mike’s long post to get to it, so I thought it important to give it a column of its own.

Eades writes about a study in the American Journal of Clinical Nutrition. “This study…demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL)…” This concerns doctors, he says, since “most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL, often seen in those following a low-carb diet, could put these dieters at risk.”

So, noting that the benefits to HDL and triglycerides are offset by “this small increase in LDL-cholesterol seen in those following a low-carb diet,” Eades wondered how the LDL in the study was calculated; the “Methods” link in the study provided the answer: the Friedewald equation: LDL = TC – HDL – TGL/5. IT IS CALCULATED! What’s that you say? It’s not a DIRECT measurement? No, and every standard lab lipid test uses this method.

But, when Friedewald, et al. developed the formula in 1972, they made an exception for people who had a triglyceride number >400mg/dl; however, since most people’s test results were in the 150 – 250mg/dl range, they made no exception for TGL values of <100mg/dl. And as readers here know, people who follow a Very Low Carb or LC/HF diet usually have TGLs in the range of 40 – 90mg/dl. The average of my last 50 is 54mg/dl.

So, Eades searched the archives for scientific papers describing differences between calculated and directly measured LDL-cholesterol in people with low triglycerides. And lo and behold, he found two! One was a case presentation where a 63yo man had a TC of 263, an HDL of 85 and a TGL of 42.  The Friedewald calculated LDL was 170 but it was just 126 when measured directly. Another paper concluded, “Statistical analysis showed that when triglyceride is <100mg/dl, calculated LDL is significantly overestimated (12.17mg/dl average).”

In addition to the over calculation of LDL cholesterol for low-carbers who have TGLs consistently <100mg/dl, Eades reminds us that low-carbers typically have the large fluffy, good type of LDL, not the small, dense type.

Dr. Mike sums this up better than I could: “The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL.  Demand to have a direct measurement of your LDL done.”

And the coup de grace: “Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish.  Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.”

Type 2 Nutrition #405: LDL-C and TGL while Fasting

One of the speakers at Keto Fest in New London last July was Dave Feldman, a self-described engineer, software developer and entrepreneur. He made a rather geeky presentation about his high LDL-C. My notes from his talk: “LDL-C has many jobs.” “Its primary job is to distribute energy from fat” (triglycerides or TGL). “Multi-day fasting before a cholesterol test will likely spike your LDL-C.” That last sentence got my attention.

Then I saw that both Michael Eades (proteinpower.com) and Jason Fung (intensivedietarymanagement.com) had also credited Feldman on this hypothesis. It turns out he’s attracted a lot of attention in the Low Carb/High Fat and fasting worlds. Here’s a related sample from Feldman’s website, cholesterolcode.com/.

“There’s just a few of us that think the same thing as I do. That cholesterol is the red herring. That mostly, this is due to higher demand for fat-based energy coming from storage in the form of triglycerides being carried by VLDLs. The cholesterol being measured resides in those VLDL-originating LDL particles, which is why its quantity is inverted from the total amount of dietary fat I eat.

More fat in my low carb diet? Less need for fat-based energy from storage, less VLDLs mobilized, less cholesterol riding along with it. Lower cholesterol score.

Less fat in my low carb diet? More need for fat-based energy from storage, more VLDLs mobilized, more cholesterol riding along with it. Higher cholesterol score.”

THE TAKEAWAY: “MULTI-DAY FASTING BEFORE A CHOLESTEROL TEST WILL LIKELY SPIKE YOUR LDL-C.”

My doctor’s appointment is typically on a Tuesday, and I generally don’t fast on weekends, but I often do on Monday. So, I made a mental note to be sure to eat fat on any fasting Monday before an appointment. Check!

I should also note that Dave Feldman is also what is known in lipidology medicine as a “hyper-responder.” “The term, ‘hyper-responder,’” Feldman says, “has been used within the ketogenic/low carb, high fat (keto/LCHF) community to describe those who have a very dramatic increase in their cholesterol after adopting a low carb diet.” This is not common, but occurred to Feldman and is the reason he began his investigations and developed “The Feldman Protocol,” a hypothesis to explain this “inverse correlation.”

Dave’s Protocol is much too complex for this blog, but if you happen to be one of the few to whom this has occurred, I strongly encourage you to click on the link above and delve into the substance of his experiments.

For my part, eating just Very Low Carb (without fasting), my LDLs and TGLs have all been very good. I wrote about them a few years ago here, here and here. Note in my case, by following a strict VLC diet, TGLs dropped about 2/3rds and HDL more than doubled. I also recently did a 14-year TGL average of 50 tests, beginning 1 year after I started VLC, and the result was 54mg/dl. The average of 15 or so in the early years was 49mg/dl.

Since starting full-day fasting, my TC has gone from 198 to 201 and then 196. My HDL-C has gone from 85 to 74 and 74. My LDL-D has gone from 101 to 114 to 100; my TGLs have gone from 60 to 67 to 108. Hmmm. Also, my blood pressure has gone from 130/80 to 125/70 and 120/80. And my A1c has gone from 5.8 to 5.3 and 5.2. This is the “expected” (default) response to switching from the low-fat, very high carb Standard American Diet to a Low-Carb/High-fat diet. Dave Feldman’s hyper-responder response is not typical, but his work on investigating the mechanism is interesting and may prove useful in explaining these (and my) anomalies.

It explains to my satisfaction, at least, my rise in TGL from my historic low averages (49 and 54) to my most recent 108. Since TGLs are a surrogate for VLDL, this corroborates Feldman’s premise given above: “higher demand for fat-based energy coming from storage in the form of triglycerides being carried by VLDLs…”