Keto – 1 Month Review

About a week and a half ago – 3 weeks into eating a LCHF diet – I added high intensity interval training (HIIT), as often as time permits, which isn’t much – I think I’ve had 4 sessions since I started.  I do 30 seconds of running uphill (5.5 mph, 6% incline), and then 4 minutes of slow walking (2 mph, 0 incline).  Repeat 4 more times.  So really I’m doing only about 5 minutes of hard work per week.  Since I started this I’ve lost 5 pounds and my fasting blood sugar has dropped from around 114, where it’s been stuck for 3 weeks, to about 102.  Post-prandial blood sugar (at 2 hours) is usually in the 80s.

I’m sleeping better, I have more energy, my mood is better than when I was eating carbs every day.

My usual diet:

  • Breakfast: eggs (1 whole egg plus 2 egg yolks cooked in coconut oil) and 1/2 of an avocado.  Sometimes a couple ounces of meat if I’m particularly hungry, but I notice ketones drop quickly if I eat too much protein.
  • Snack (because I can’t make it the 6 hours till lunch without one): bulletproof coffee (16 oz coffee with 2 Tbs unsalted grassfed butter and 2 Tbs MCT oil.  Yes, I’m using the actual, authentic mycotoxin-free upgraded coffee from Mr. Bulletproof himself).
  • Lunch: 1/2 avocado, 1-2 Tbs. homemade mayo, about 4 oz of chicken/fish/steak, a bunch of kalamata olives.
  • Snack – whatever coffee is still in my thermos, maybe some macadamia nuts
  • Dinner – a small-medium portion of whatever my family eats – last night it was cod cooked in butter.  I have been avoiding the veggies to see if it makes a difference one way or the other.

I’m hungriest in the morning, and have been eating till I’m not hungry anymore.  I might experiment with getting rid of that last egg white, and see if that reduces hunger by reducing impact on insulin levels.

Current supplements:

Medications:

  • Hydrochlorothiazide – 25mg/day (for hypertension)
  • Methyldopa – 250mg 3x/day (for hypertension)

I quit taking the Metformin.  It made my breasts stupid big and really sore and after 3 weeks it just wasn’t going away.  I figured I could manage without it eating Keto anyway.  So it’s gone.  Now, a couple weeks later, my bras still don’t quite fit.  Hot flashes are starting to come back as hormone levels return to baseline.

Marriage update:  Things are on cruise control.  It’s a real pain in the ass to split up.  For now, we’re just getting through the day to day, no movements in that direction.  He doesn’t want to split up and I’m not sure my life would be better if we did.  We get along well so it’s not painful.  Not the marriage I thought I had, but many things in my life are wonderful, so this is fine for now.

A request was made for my extremely easy homemade mayo recipe.  I have to admit it’s not MINE, exactly, because I got it from here.  I did tweak it a little so I’ll share the recipe as I make it:

Coconut Oil Mayonnaise

Equipment:

  • 1 glass jar with a mouth wide enough to accommodate a stick blender. I’ve used Vlasic dill pickle jars and 16-oz wide mouth Mason jars.  Both are great.
  • A stick blender (I use this one).

Ingredients:

  • 1 egg
  • 1 cup of fractionated coconut oil (the kind that is liquid).  I use Carrington Farms, which is available at Walmart.
  • 1 Tbs lemon juice (more if you like it a little more sour)
  • 1/4 tsp salt

Instructions:

  • Put everything in the jar.
  • Get the stick blender and put it in the jar, resting it on the bottom of the jar.
  • Hold on to the jar.  (<– Once I didn’t do this and the jar spun right off the counter onto the floor.  A serious waste of good ingredients).
  • Turn on the blender for 20-30 seconds, moving it up and down a little to incorporate all of the liquid into the emulsified mayo.
  • Done!  Refrigerate for up to 2 weeks.

Some info about fractionated coconut oil is here.  Apparently it is liquid at room temperature because the long-chain fatty acids are removed, along with some of the health benefits of coconut oil.  I made the mistake of trying this recipe with regular (melted) coconut oil once and found myself with an unacceptably solid final product.  The fractionated oil works well for this recipe, and still has the health benefits associated with MCT oil, without the PUFAs found in other liquid oils.

I’ve tried this recipe with other oils.  Olive oil (“extra light”) tasted good but even good olive oil is 12% PUFA.  The same is true for avocado oil, though I never tried that one.  I tried it once with regular olive oil (not the “extra light”), and it tasted way too strong.  I tried making it in a bowl once, rather than in a glass jar…it didn’t emulsify.  It needs to be in the narrower container to come together.  I already mentioned my foibles with using regular coconut oil and letting the jar spin out of control….Ok, I guess that’s it. The recipe and instructions above has never let me down.

Oh and speaking of PUFA…check this out.  Michael Eades, a long-time leader in the low-carb community seems to be turning his attention away from blaming sugar and towards the evils of PUFA.  Very interesting.  And score one for Ray Peat.

Upswing

Ok, I’m feeling better again.  No more!  No more crazy anything!  I’m just going to accept that I’m fat and get about the business of feeling better.  Forever.  No more deviations from the plan. I’ve been eating a lot of garlic, trying to make the endotoxin die down.  I think I’ve managed to poke enough holes in my intestine now from various experiments (let alone my unhealthy pre-Peat life), and now I accept that I don’t EVER get to eat starches and I don’t EVER get to eat fibrous fruits and veggies.  For at least…oh, a year or so.  Then MAYBE once a week or once every 2 weeks I can have an apple or a serving of potatoes.  But now, NO.

I recovered my energy and my mood by eating non-fibrous whole fruit, juice, meat, and lots of dairy (all forms).  Not gonna fuck it up again.  NOT GONNA.  YOU HEAR ME ENDOTOXINS?  YOU SUCK.

On another note…

One of my favorite bloggers in the entire world, Ray Medina, has moved his website to here.  I was poking around his site and came across this excellent article called Ulcerative Colitis and Dietary PUFAs.  I don’t have UC so I would normally have skipped right by it, but for some reason I decided to read it.  He discusses a mouse experiment that really makes a great case for avoiding omega 3 fatty acids.  In fact, I’ve never really understand the Peatarian assertion that Omega 3s only APPEAR to be good for you by “suppressing the immune system.”  This article explains it really well.  In essence, if you eat a diet high in PUFA, adding some Omega 3s (or fish oil) will make your labs look better.  BUT YOU’RE ALSO MORE LIKELY TO DIE SOONER.  hahahaha.  Good stuff.

Go read it.  And then stop eating salmon.

The end.

Peat vs PHD: A Comparison

Ok, I finished the Perfect Health Diet (PHD) book by Paul Jaminet and his wife, Shou-Ching Jaminet (I notice she doesn’t get much credit in PaleoLand, but she’s the co-author and also a Ph.D.). I was drawn to it in the first place because they advocate a moderately low-carbohydrate diet (just enough carb to meet the body’s needs, which they say is around 600 calories or 150g per day), and that a good chunk of those carbs should be starches, which I’ve recently started eating.

I thought it would be fun to compare the recommendations made by Ray Peat and those made in the PHD. First, let’s look at the similarities.  They both recommend a whole-food diet, liver once a week, shellfish once a week, and both caution to avoid PUFAs, grains (though both seem to make exceptions for rice), and legumes.  Peat says keep PUFAs low – real low – like 1-2% of your dietary calories low.  The PHD says under 4% is probably ok. Potatoes seem to be ok with both of them.  Both say that saturated fats are awesome – butter, coconut oil, and cream being fabulous in both camps. Both are fairly noncommittal about non-starchy vegetables: Peat says they’re ok if they’re well-cooked, but I get the distinct impression he finds them fairly optional, and the PHD says you can eat around a pound per day of non-starchy veggies, but there’s no firm guideline.  They say, “Eat vegetables to taste – they are nourishing and add flavor to meals – but don’t consider them a calorie source.” (PHD, KL 3217). Both recommend getting lots of your nutrients from liver, shellfish, eggs and bone broth.

Ok, that’s about where the similarities end.  The greatest areas of disagreement between Peat and the PHD are with regard to calcium/dairy/phosphorus, fructose/sugar, and Omega 3s.  Peat strongly recommends getting enough dietary calcium to maintain between a 1:1 and a 1:2 ratio of calcium to phosphorus, ideally closer to the former. His views on this topic are expressed well here:

A diet that provides enough calcium to limit activity of the parathyroid glands, and that is low in phosphate and polyunsaturated fats, with sugar rather than starch as the main carbohydrate, possibly supplemented by niacinamide and aspirin, should help to avoid some of the degenerative processes associated with high phosphate: fatigue, heart failure, movement discoordination, hypogonadism, infertility, vascular calcification, emphysema, cancer, osteoporosis, and atrophy of skin, skeletal muscle, intestine, thymus, and spleen (Ohnishi and Razzaque, 2010; Shiraki-Iida, et al., 2000; Kuro-o, et al., 1997; Osuka and Razzaque, 2012). The foods naturally highest in phosphate, relative to calcium, are cereals, legumes, meats, and fish. Many prepared foods contain added phosphate. Foods with a higher, safer ratio of calcium to phosphate are leaves, such as kale, turnip greens, and beet greens, and many fruits, milk, and cheese. Coffee, besides being a good source of magnesium, is probably helpful for lowering phosphate, by its antagonism to adenosine (Coulson, et al., 1991).

The PHD barely mentions phosphorus.  A search of the Kindle version of the book indicates it’s mentioned 7 times within the body of the text, each time as part of a list of nutrients (e.g., “magnesium, calcium, and phosphorus…”).  There’s no discussion at all about potential deleterious effects associated with high phosphorus intake.  It’s interesting because overall the PHD does a great job of describing deficiencies and toxicities of all of the main micronutrients.  They didn’t touch on this one though.  The calcium/phosphorus ratio recommended by Peat is one of the things I’d never heard before I began studying his work.  He says that calcium gets blamed for a lot of negative effects in the body when phosphorus is the real culprit.

The PHD talks about the effects of too much calcium, citing studies that indicate 600mg per day is adequate and maximizes bone health (PHD, KL 5175).  It goes on to say:

Calcium supplementation was a mistake.  The true culprits in osteoporosis are deficiencies of Vitamin D, Vitamin K2, and magnesium.

and…

Studies have found that supplemental calcium increases the incidence of strokes and heart attacks by over 30 percent and increases the overall risk of death by 9 percent. One analysis concluded, “Treating 1,000 people with calcium or calcium and vitamin D for five years would cause an additional six myocardial infarctions or strokes and prevent three fractures. (PHD, KL 5183)

It goes on to blame calcium for brain lesions, the promotion of biofilms, and hypercalcemia.  Apparently this study found that calcium balance occurs at an intake of 741mg/day – that’s the amount of calcium retained by the body each day. So that’s what the PHD recommends – about 700mg/day, in the form of bone broth, green leafy vegetables, maybe some dairy.  The PHD was kinda wishy washy on the dairy thing.  They didn’t give it a section in the book, which I find odd.  I mean, “Alcohol” had it’s own section. Lots of people eat dairy and to not really acknowledge it doesn’t make sense to me.  Plus in the beginning “Milk” is listed among the items to avoid, “…but DO eat fermented or fatty dairy products: butter, sour cream, ice cream, cheese, yogurt,” (PHD, KL 198).  I should avoid milk (and sugar!) but ice cream is ok?  Kinda loopy.

Ok, so Peat says we’re gonna die if we don’t get enough calcium, and PHD says we’re gonna die if we get too much.

Another big area of disagreement between these guys is with regard to fructose. The PHD says fructose is only bad in high doses or when eaten with PUFAs – but since most Americans eat a high-PUFA diet, it’s a big deal on a societal scale.

Fructose appears most problematic when study subjects are obese or overweight and when they are eating diets high in polyunsaturated fat.” (PHD, KL 3904)

The PHD goes on to say that fructose is toxic to the liver and causes metabolic syndrome, diabetes, endotoxemia, poor blood lipid profile, high uric acid (an aside: my uric acid went DOWN on a higher-fructose diet), gout, kidney disease, obesity, liver disease, cognitive impairment, and retinopathy.  Still though, they recommend up to 25g of fructose per day, and at most 10g per meal.  The dose makes the poison, apparently.  Keep your PUFAs low and a little is fine.

Peat says fructose has been wrongly maligned:

Many people lately have been told, as part of a campaign to explain the high incidence of fatty liver degeneration in the US, supposedly resulting from eating too much sugar, that fructose can be metabolized only by the liver. The liver does have the highest capacity for metabolizing fructose, but the other organs do metabolize it.

If fructose can by-pass the fatty acids’ inhibition of glucose metabolism, to be oxidized when glucose can’t, and if the metabolism of diabetes involves the oxidation of fatty acids instead of glucose, then we would expect there to be less than the normal amount of fructose in the serum of diabetics, although their defining trait is the presence of an increased amount of glucose. According to Osuagwu and Madumere (2008), that is the case. If a fructose deficiency exists in diabetes, then it is appropriate to supplement it in the diet.

And regarding the effect of fructose on obesity:

Starch and glucose efficiently stimulate insulin secretion, and that accelerates the disposition of glucose, activating its conversion to glycogen and fat, as well as its oxidation. Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat. Eating “complex carbohydrates,” rather than sugars, is a reasonable way to promote obesity. Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten. The obesity itself then becomes an additional physiological factor; the fat cells create something analogous to an inflammatory state. There isn’t anything wrong with a high carbohydrate diet, and even a high starch diet isn’t necessarily incompatible with good health, but when better foods are available they should be used instead of starches. For example, fruits have many advantages over grains, besides the difference between sugar and starch. (Emphasis his.)

I can say my own experience of eating sugar (mostly fructose/glucose in fruit juice and honey) did not result in fat production – my weight was stable the entire time I avoided starches. So score one for Peat. However, I was hungry all the time. And in the past week or two of eating starches it has NOT been the case for me that they stimulate my appetite. I can forget about eating now for the first time in months – what a relief.  Starches do make me sleepy though.

Speaking of which, I’m getting tired…time to wrap this up!

The last big area of disagreement seems to be regarding Omega 3 fatty acids – should we eat salmon and other fatty seafood or not?  Peat says NO, PHD says YES (once a week).  I’ll go into this in greater detail in another post. I have more reading to do on this topic.

My conclusions (for me): I think I’m going to keep eating dairy.  Peat makes a better case.  And I think I’ll avoid fructose – not because of what the Jaminets have to say, but because I don’t particularly like fruit and I don’t miss it at all…and because it did seem to mess up my lipid profile to a point that I’ve become concerned…but seriously, I’m pretty broken.  It probably doesn’t take much to tip those scales into the danger zone.  As for omega 3s – the jury is still out. So dairy is a YES, with phosphorus limited relative to calcium intake.  Fructose, for me, is a NO. But just cuz I don’t like it. You go ahead. Just keep your PUFAs low and you’ll probably be just fine.

Reconsidering Low Fat

I emailed Ray Peat yesterday to get his opinion about my “Does-saturated-fat-cause-high-blood-sugar?” experiment.  I asked him if it was indeed the case that too much saturated fat in one’s diet could cause impaired cellular glucose uptake.  I’ve never written to him before, and felt nervous about doing so.  I felt like a kid writing to John Lennon or something.  He wrote back in about 20 minutes and said:

Butter, cream, and coconut oil are the only common food fats that are mostly saturated, and because coconut oil is oxidized more quickly than most fats, it’s the least likely to block sugar oxidation. Any long chain fat can interfere with sugar oxidation, but the polyunsaturated fats, such as in poultry, fish, and pork, are more water soluble, and slower to be oxidized than saturated fats, and they affect hormones and other regulatory systems differently, so they interfere a little more strongly.

He also sent me the abstracts for a few relevant studies (cited at the bottom of this post).

I’ve been thinking today about my experiment.  I did a statistical analysis on the data I collected (fat grams eaten vs. fasting blood sugar) and the data showed a moderate correlation between the two variables (r=0.42).  If you’re familiar with statistics, you know that 1.0 is a perfect correlation – when X increases, Y always increases, and when X decreases, Y always decreases.  A correlation of r=0.0 means there is no meaningful relationship between the two variables.  So a correlation of r=0.42 is a reasonable correlation – but because I didn’t have enough data points (days) it wasn’t statistically significant – meaning, it could have been just chance that made my graph look the way it did.  Another week and it would have been statistically significant.

So pondering today, I’m thinking, this is my health here, and my hyperglycemia is one of my biggest health concerns.  I really just need to get over my whininess about eating too many sweet things and give this a good solid trial.  No confounders – just eating low fat and monitoring my blood sugar.

So I’m going to do that, starting tomorrow, and I’m going to do it for at least 3 weeks.  Hopefully longer.  I’m not going to make any conscious effort to eat low-calorie.  Just low fat.  By low-fat, I mean I’ll keep fat under 20% of my total calories per day.  If things are going well, I may go lower, but I’ll consider each day a success if I can do that.  Fat calories will be coming largely from coconut oil.  My diet will be centered around fat-free dairy, fruit, juice, lean meat, broth, honey, coffee, eggs, salt, liver, shellfish, and gelatin.  I may need to eliminate cheese for a while.

It occurs to me that if I can manage to do this – prove at a level of statistical significance that a low-fat high-sugar diet fixes diabetes – well, that would really be something.  I hear stories of people having done this, but I don’t know of anyone who has made their story public so others could learn from it and try it themselves.

So tomorrow begins….The Great High Sugar Low Fat Diabetes N=1.

____________________________

Citations provided by Ray Peat:

Proc Natl Acad Sci U S A. 1988 Aug;85(16):6137-41.
Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced
diabetes in CD-1 mice.
Wright JR Jr, Lefkowith JB, Schreiner G, Lacy PE.
Author information:
Department of Pathology, Washington University School of Medicine, Saint Louis,
MO 63110.
Multiple i.p. injections of low-dose streptozotocin (40 mg/kg) produce insulitis,
beta cell destruction, and diabetes in male CD-1 mice. Recent data also suggest
that macrophages figure in the low-dose streptozotocin model. Because other
recent studies have shown that essential fatty acid deficiency prevents
autoimmune nephritis in mice, decreases the number of resident Ia-positive
glomerular macrophages, and decreases the elicitation of macrophages into the
glomerulus in inflammation, we examined the effect of essential fatty acid
deficiency on the incidence and severity of insulitis and diabetes in CD-1 mice
treated with low-dose streptozotocin. Streptozotocin-treated mice on the control
diet uniformly developed diabetes (19/19). Essential fatty acid-deficient mice
treated with streptozotocin did not develop diabetes (1/13). Mean plasma glucose
levels for the control and essential fatty acid-deficient mice were 384.5 ±
23.6 and 129.1 ± 15.5 mg/dl, respectively, at the end of 1 month. To discern
whether essential fatty acid deficiency prevented the streptozotocin-induced beta
cell injury or the inflammatory response to injured beta cells, mice were
repleted with daily injections of 99% pure methyl linoleate beginning 3 days
after the last streptozotocin injection. These mice also quickly developed severe
(3/4) or mild (1/4) diabetes. Histologic examination of the pancreata of control
mice or repleted mice showed marked insulitis and beta cell destruction; in
contrast, the pancreata of essential fatty acid-deficient mice showed
preservation of beta cells and only focal mild peri-insulitis. Essential fatty
acid deficiency thus prevents the insulitis and resultant diabetes in low-dose
streptozotocin-treated CD-1 mice, suggesting a central role for macrophages and
lipid mediators in this autoimmunity model.

Acta Diabetol. 1995 Jun;32(2):125-30.
Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced
diabetes in naive and cyclosporin-treated low-responder murine strains.
Wright JR Jr, Fraser RB, Kapoor S, Cook HW.
Department of Pathology and Surgery, Izaak Walton Killam Children’s Hospital,
Halifax, Nova Scotia, Canada.
We have previously shown that essential fatty acid (EFA) deficiency prevents
diabetes and ameliorates insulitis in low-dose streptozotocin (LDS)-treated male
CD-1 mice. The effects of EFA deficiency on the incidence of diabetes after LDS
treatment has not been examined in other strains. In contrast to highly
susceptible CD-1 mice, several other strains of mice are only partially
susceptible to LDS treatment and do not develop appreciable insulitis; however,
the susceptibility of these strains can be markedly increased by cyclosporin A
(CsA) pretreatment to reduce suppressor cell function. Weanling male BALB/cByJ,
DBA/2J, and C57BL/6J mice were placed on EFA-deficient (EFAD) or control diets
for 2 months and then divided into experimental and control groups. Ten EFAD and
10 control mice from each strain received LDS treatment (40 mg/kg/d 5 d); an
additional 10 EFAD BALB/cByJ and another 10 control BALB/cByJ mice received
subcutaneous CsA injections (20 mg/kg/d) for 14 days prior to and for 5 days
simultaneous with LDS treatment (40 mg/kg/d 5 d). Plasma glucose levels for all
mice were determined 3 times per week for 3 weeks after LDS treatment. Mean
plasma glucose levels (+/- SEM) at the end of the experiment were significantly
lower in the EFAD groups vs control groups in BALB/cByJ (P < 0.001), DBA/2J (P <
0.00001), and C57BL/6J (P = 0.012) mice. CsA supplementation increased the
severity of diabetes in LDS-treated BALB/cByJ mice (P < 0.0005); however, EFA
deficiency also prevented diabetes in CsA-supplemented BALB/cByJ mice.(ABSTRACT
TRUNCATED AT 250 WORDS)

Pancreas. 1995 Jul;11(1):26-37.
Essential fatty acid deficiency prevents autoimmune diabetes in nonobese diabetic
mice through a positive impact on antigen-presenting cells and Th2 lymphocytes.
Benhamou PY, Mullen Y, Clare-Salzler M, Sangkharat A, Benhamou C, Shevlin L, Go
VL.
Diabetes Research Center, UCLA School of Medicine 90024-7036, USA.
Protective effects of essential fatty acid deficiency (EFAD) on autoimmunity were
shown in rodents. Our goal was to investigate the mechanisms of EFAD effects on
autoimmune diabetes in nonobese diabetic (NOD) mice. Weanling female mice were
randomized between a control diet group and an EFAD diet group, and the
development of diabetes and immune response was determined over a 6-month period.
The cumulative incidence of diabetes was significantly reduced in the EFAD group
(20 vs 68.75% in the control group; p < 0.01), without affecting the insulitis
process. Splenocyte reactivity to phytohemagglutinin and anti-CD3 antibody was
significantly increased in EFAD-fed mice (p < 0.01). The EFAD group also
exhibited a dramatic increase in baseline (29-fold) and antigen-presenting cell
(APC)-stimulated (10-fold) T cell responses in syngeneic mixed leukocyte
reaction. These responses were associated with a marked increase in splenocyte
interleukin-4 (IL-4) production, a reduction in interferon-gamma production, and
a down-regulation of CD45RB isoform expression. Macrophages in the EFAD group
exerted a reduced suppressive effect on concanavalin A-induced splenocyte
proliferation and were found to release increased amounts of tumor necrosis
factor-alpha and IL-1 and reduced amounts of prostaglandin E2. These results
clearly demonstrate that EFAD prevents diabetes in NOD mice. The data suggest an
enhanced activity of Th2-like cells, as well as an effect on APC activity linked
to alteration in eicosanoid metabolism.

Prostaglandins Leukot Med. 1986 Aug;23(2-3):123-7.
Essential fatty acid deficiency: a new look at an old problem.
Lefkowith JB, Evers AS, Elliott WJ, Needleman P.
Essential fatty acid (EFA) deficiency is a useful tool to study the role of
arachidonate and its metabolites in various physiologic and pathologic states.
Recent studies have clarified the effects of EFA deficiency on membrane
arachidonate and its metabolites, and have demonstrated that 20:3(n-9) (which
accumulates in EFA deficiency) can be metabolized to a variety of eicosanoids.
EFA deficiency has been shown to exert an anti-inflammatory effect. The mechanism
of this effect may in part be mediated through a decrease in leukocyte
leukotriene formation. In contrast, studies using the novel fatty acid,
columbinic acid, have shown that the epidermal dysfunction seen in EFA deficiency
may be a function of linoleate and its lipoxygenase metabolites rather than of
arachidonate and the prostaglandins. Finally, it has recently been shown that EFA
deficiency potentiates the effects of volatile anesthetics. EFA deficiency may
thus provide a useful tool to investigate the molecular mechanism of these drugs.

J Lab Clin Med. 1981 Nov;98(5):764-75.
Effects of experimental diabetes on the essential fatty acid-deficient rat.
Riisom T, Johnson S, Hill EG, Holman RT.
An evaluation of the EFAD syndrome in rats rendered diabetic with either alloxan
or streptozotocin was performed. Diabetic rats fed an EFA-deficient diet for 7 or
13 weeks were less severely EFA-deficient than were nondiabetic rats fed
EFA-deficient diet, as judged by dermal symptoms or by biochemical parameters
such as the ratio of 20:3 omega 9/20:4 omega 6 (T/T ratio) and total fatty acids
derived from linoleic acid. The T/T ratios of liver PL of diabetic EFA-deficient
rats were lower than those of deficient control rats, and the ratios varied
inversely with the blood glucose concentrations. The product/precursor ratios,
arachidonic acid/linoleic acid, in liver PL were higher in diabetic deficient
rats than in deficient control rats. Analysis of liver and heart PLs revealed
higher arachidonic acid levels in the diabetic deficient rats than in the
EFA-deficient controls, perhaps because of different growth rates. The activities
of the delta 5, delta 6, and delta 9 desaturases were evaluated in liver
microsomal systems. The delta 9 desaturase was depressed in diabetic rats in
agreement with literature reports. The delta 6 desaturase, however, was slightly
increased. The relative levels of delta 5, delta 6 and delta 9 desaturation
products in liver and heart PLs did not parallel the measured desaturase
activities of liver microsomes.

Two Steps Back

I’ve been struggling a bit eating Peat style.  I think this would be a great way of eating if weight loss isn’t a goal.  The food is delicious and makes me feel great.  Only problem is I’ve been gaining weight.  I’m now up to 209.4 – almost 8 pounds over my previous unacceptable weight prior to learning about Dr. Peat.

It has to stop.  I simply cannot continue to gain weight.  My clothes don’t fit.  I avoid mirrors.  I’m discouraged.  I’ve tried to count calories, and I find it impossible to stay on a low-calorie diet while eating sugar.  There’s one woman on my Ray Peat Facebook group who has been losing weight, and she has generously shared her eating plan with us.  I’ve tried to follow it, and I just can’t.  I feel too hungry.  I guess my body is just not healthy enough yet to metabolize sugar effectively.  I think a lot of the sugar I’m eating is being wasted, my liver not effective at storing glycogen.

I’m considering doing a lower-carbohydrate version of Peat’s principles for a couple of months (and yes, I realize “a lower carb Peat plan” is an oxymoron) – just long enough to get some of the weight off.  I think my low-carb diet didn’t result in weight loss before because I was eating too much meat and no dairy. Also I was eating lots of PUFAs in daily consumption of dark-meat chicken and conventional eggs.  Now that I see how damaging those things are, of course I would continue to avoid them.

I don’t know all the answers.  I just need to do something else. I can’t continue to gain weight.

Score 3 for Ray Peat

Yesterday I decided to do some blood glucose (BG) testing while drinking orange juice.  I’ve been turned off from OJ because I tested my BG after drinking it in the morning and it was high – like in the 170s.  I tested again in smaller quantities, but I always felt really hungry after drinking just a little so what’s the point?  Well, I’ve since learned that the hunger you feel when you eat fruit is your true hunger.  Low carb dieting raises stress hormones, which reduce appetite.  No wonder people lose weight on low carb – their cortisol is suppressing their drive to eat.  Until 6 months later when they (might) realize their thyroid doesn’t work anymore.  Anyway, hunger means there are no stress hormones running around, so eat, dummy.  One problem with this though – I have been hesitant to keep eating juice or fruit because I didn’t want my blood sugar to be high all day. What a conundrum!

Well, I decided to turn to science to get some answers.  I drank 12 oz of orange juice at breakfast and then 3-4 oz every hour.  Here were my readings:

  • Fasting blood sugar: 127; Temp/pulse 98.1/79
  • 9:00AM – 172
  • 10:00AM –  139
  • 11:00AM – 115 (temp/pulse was 98.6/79)
  • 12:00 – 115
  • 1:00 – 74 (after 30 minutes mild/moderate exercise)
  • 2:00 – 97
  • 3:00 – 106

Huh.  So for some reason there’s a big spike at first but then blood sugar is low all day.  Weird!  I did it again today to see if the results would replicate.  Had breakfast with about 10oz juice.  Here’s what I got:

  • Fasting – 124; temp/pulse 98.0/85
  • 9:00AM – 119 (tested at 1 hour and 20 minutes after breakfast)
  • 10:00AM – 106 (temp/pulse 98.8/75)
  • 12:00 – 101
  • 1:00 – 107
  • 2:00 – 112

At that point I stopped testing every hour.  Good enough!  I did take one more test though, after 30 minutes of stationary biking.  Blood sugar was 72, similar to the previous day after biking.  I thought it was weird that I didn’t feel hungry at all with blood sugar that low.  Then I remembered…About 10 years ago I used to do martial arts (Aikido).  I would train hard for an hour and a half, and leave the dojo feeling really good, but not hungry.  Then about an hour later I would become ravenously hungry.  Now I understand why!  The workout was causing a stress response – cortisol and/or adrenaline were suppressing my appetite.  After relaxing for an hour or so the stress hormones would lower and my true hunger would be revealed.  This is why Peat (and others) are opposed to exercise – it raises stress hormones.  I guess I knew this intellectually, but it makes a lot of sense now having experienced a complete lack of hunger after exercising, while my blood sugar is getting very low.  Interesting.  I’ve been doing 30 minutes of biking and 15 minutes of yoga per day for the last week.  Maybe instead I’ll do 30 minutes of yoga and 15 minutes of weight lifting.  Less continuous stress.

The other thing on my mind has to do with progesterone.  Ray Peat did an interview that was aired last week, in which he answered lots of questions that had been submitted by listeners.  Well, prior to the interview I submitted a question.  My question appeared in the second hour of the interview, and was as follows:

I’ve recently started taking Progest-E, and it has helped my cyclical mood symptoms very much.  I’ve been taking it days 14-28 of my cycle.  I hate to stop taking it because I have PMS (moodiness) the day after I stop.   Would there be any harm in just continuing to take it non-stop for a while, even if it means I miss a period or two?

Dr. Peat’s answer:

I’ve known quite a few women who took it every day and kept cycling without any problem.  But what they should be aware of is that if you take a little bit extra just before the expected time of ovulation it will trigger early ovulation, and then if you stop taking it or take less it will bring on an early menstruation.  So if you’re going to take it every day, it has to be every day the same amount.

If you’ll remember I really REALLY didn’t want to stop taking my Progest E after day 28 last month. In fact, I kept taking it and taking it and finally stopped against my will to have a period.  Then I started up again on Day 4 of my cycle – a full 10 days before I was supposed to start up – because the symptoms of high estrogen were unbearable.  I was depressed, bitchy, and puffed up.  It sucked.  So I started my progesterone early.  Well, surprise surprise…my period came 10 days early.  And it’s very possible I dosed a little too high before ovulation.  That Ray Peat.  He sure does know some stuff.

More news: after about 10 days of probiotics my gut is still messed up.  I tried taking two teaspoons of potato starch today (far less than the 4 Tbs many people are downing at one time) and still…not good. Gut mad at me.  I don’t know what it will take to fix what is wrong, but I’ll continue with the probiotics for now.

And the orange juice…3-4 oz an hour.

Oh one more thing – suddenly my body is ok with cheese.  I have completely stopped eating fatty chicken and most eggs, cutting my PUFA intake to almost nothing.  Could that be why my asthma isn’t kicking my ass right now?  I had like 4-5 oz of cheese today…and no problems.

Ok, blood sugar…progesterone…and PUFA.   I can’t deny it any more.  All the crap he says is coming true for me.

I think Ray Peat is right.

Starches, Sugar, Diabetes, and PUFA

Every so often I get research fatigue.  It’s the head-spinning sensation that comes with reading endless contradictory information about health, diet, exercise, and nutrition.  Red meat – high in heme iron (so it’s bad!) but high in carnitine and low PUFA (so it’s good!).  Dairy – high in iodine (so it’s bad!), but high calcium to phosphorous ratio (so it’s good!). Fructose – increases triglycerides (so it’s bad!), but increases metabolism (so it’s good!) but causes weight gain (so it’s bad!) but has a lower effect on insulin (so it’s good!).  I can’t stand it anymore.

My weight has been up and down a lot – now it’s up.  I’m not feeling good anymore.  I don’t know if my feelings of well-being associated with eating Peatarian were just a month-long diabetic sugar high or if something positive was actually happening metabolically.  I’ve been experimenting with potatoes, trying to find a way to get some carbs in and also keep my blood sugar stable.  Eating 1/4 cup of boiled potatoes, along with protein and fat, keeps me from having blood-sugar swings…but also makes me feel dull and lethargic.

Today I listened to Ray Peat’s interview called Glycemia, Starch, and Sugar, in Context.  I was driving at the time (for 3 hours, through a blizzard I might add), so I couldn’t take notes, but what I took from it is the following:

  • Diabetes is caused by Polyunsaturated Fatty Acids (PUFA) in the diet and in the system.  Stop eating PUFAs and within a couple days you’ll be more insulin sensitive.
  • Potatoes have some unique and magical properties, but the magic is in the juice – not in the starch.  If you juice a raw potato and drink (or cook with) the juice, there are ketones (or ketone acids?) available that are very healing and can perform miracles like make insomniacs sleep and heal severe digestive problems.
  • The problem with low-carb diets is the following:  The body releases insulin to process the amino acids in proteins.  When insulin rises, the body needs to raise blood sugar to avoid hypoglycemia.  If there’s no glycogen (sugar) stored in the liver cortisol is released instead, which increases blood sugar.  Cortisol suppresses thyroid function and immune function, and lowers metabolism.
  • Starches can cause bacterial problems in the gut.
  • Fructose is misunderstood and is awesome.

There was more, of course, but listening from my own insulin-resistant context, this is what I heard.

I haven’t done a great job of getting PUFAs out of my diet.  I keep eating chicken.  I should stop doing that.  It’s worth a try, to see how much of a difference it would make for me to stop that.  I’m not even sure why I do.  (Edited to add my inner monologue after I hit “Publish”:  I know why I do.  I really like meat – I like that it keeps me from being hungry.  I hate being hungry.  And chicken is inexpensive. I can’t even believe how much money we spend on food already.  If I upgraded to higher-quality meat I’d have to get a full-time job again. Seriously. Ok, instead, I’ll work on eating less meat, more dairy, more gelatin for protein.  /moment of self-awareness)

I’m tired of thinking about it.  For now.

No more PUFA for me.

Diabetes

I didn’t do a glucose tolerance test.  Jenny Ruhl, who manages this informative site says the following about diagnosing diabetes:

If your blood sugar went over 200 mg/dl (11.1 mmol/L) at any time you tested, you just registered a diabetic blood sugar level and should consult with a doctor as soon as possible. Two random tests results of 200 mg/dl are considered diagnostic of diabetes according to the Diagnostic Criteria for Diabetes Mellitus published by the highly conservative American Diabetes Association.

Yesterday my blood sugar was almost 300…and over 180 at the 2 hour mark after eating.  It wouldn’t be hard for me to get the same result again, I don’t think.

So I guess I’m diabetic.  The time during which I ate low carb I was probably diabetic too…but it was managed/masked by never eating carbohydrates.

Awesome.

Tonight I listened to Ray Peat’s KMUD interview on the subject of Energy Production, Diabetes, and Saturated Fats.  Here are my notes from the interview:

On Polyunsaturated Fatty Acids:

  • “Essential Fatty Acids”  – vegetable oils, polyunsaturated fatty acids (PUFAs).  Scientific evidence is hugely against their use as a part of a healthy diet.  Cites an anecdote in which someone went on a very low fat diet and lots of symptoms improved – improvement was likely because he eliminated PUFAs that were causing problems.
  • Linoleic acid causes heart disease and cancer and it’s been marketed as preventing heart disease.
  • In the 50’s they were feeding mink lots of fish, and they developed an icky disease.  Fish oils seem to be toxic as well.  When the omega 6 oils seemed to be incriminated as causing heart disease, the omega 3s were promoted instead.  They’re both bad.
  • The safe oils are butter, stearic acid, coconut oil, palm kernel oil, beef/lamb fat, and olive oil.  Chicken fat and pork fat are as bad as corn oil because those animals (non-ruminants) are eating corn.
  • Stuff growing in the ocean has access to trace minerals, but things grown inland (e.g., farmed fish/shellfish) will be deficient in these unless they’re being given an appropriate diet (and they’re probably not).
  • Randall found that when you raise FFAs, you inhibit ability to oxidize glucose.  Stress increases FFAs, and oxidizing glucose is what you need to overcome stress.  Counterproductive.  Our systems are designed not to eat PUFA.  The PUFA turn on the stress hormones that interfere with the energy, which results in more stress hormones.  Body is designed to work on saturated fats.  We happen to be living in a time where poisonous fats are prevalent and promoted.
  • Butter turns off adrenaline, ACTH, cortisol, while corn oil turns them on.  The excitotoxic system of the brain is turned on by PUFAs.  So PUFAs = inflammation, Alzheimer’s, diabetes, block use of sugar so blood sugar remains high
  • People with cancer have lots of PUFA in their body, according to a study.  Putting rodents on a diet of saturated fat prevents/delays breast cancer.
  • Adding PUFAs shorten lives of animals with tendency toward heart disease.
  • Niacin is effective for heart disease and diabetes – lowers the FFAs.  That isn’t being promoted by anyone because it’s so cheap.
  • Liver is high in niacin, as well as other animal foods (milk, eggs).
  • Fish in the Amazon have fat that is almost as saturated as butter.
  • Cows bacteria detoxify unsaturated fats that they eat, so (I think he was saying) industrial beef is not as bad as chicken/pork.
  • Vitamin E actually destroys PUFAs.

On Diabetes:

  • Diabetes is an energy deprived state.  Alzheimer’s is becoming known as diabetes of the brain.  Inflammation = a failure of energy.   Diabetes – all you can do with glucose is make lactic acid (and you can test for this).  Doesn’t produce enough energy for normal function.
  • Diabetics are forced into fat burning mode, and that would be ok if it was saturated fat being released.  The fat cells prefer to burn saturated fat, so these get burned first.  Our tissues become more concentrated with PUFAs over time, the older we get, because that’s what’s left after the saturated fats are burned off.  Then when we’re under stress and don’t get enough sugar we have to burn PUFAs which damage mitochondria, destroy genetic material inside mitochondria, which gives rise to cancer.  This only occurs in the presence of PUFAs.
  • People who change diet take about 4 years to eliminate most PUFAs, though a thin person can change over to saturated fats very quickly.  If you eat frequently and avoid stress causing foods and don’t let self get hungry enough to have stress hormones release FFAs, you can quickly switch over to an efficient metabolism.  Frequent eating, always with sugar and always with absolutely NO PUFA, allows slow disposition of toxic fats.  Our liver treats PUFA like it treats other toxins.  If it has the energy, it attaches them to sugar and prepares them to be excreted.
  • If you lose a lot of weight quickly you’re stressing liver (high liver enzymes).  If liver stays energized (frequent feedings, good nutrition) it can slowly eliminate these fats.  But when under stress you damage cells and you knock out the enzymes that are needed to detoxify.
  • What to eat?  Fruit and cheese (the host says this…not Peat, but he agrees with it).

The Takeaway Message:  Don’t eat Polyunsaturated Fatty Acids (PUFAs).  They’re poison and they give you diabetes and cancer.  To fix your metabolism, eat frequently, always have some form of sugar, make sure nutrition is good, including niacin.  Wait up to 4 years for the damage to be repaired.

I don’t know if he’s right or not.  Jenny Ruhl says that diabetes is caused by genetics and poisons in the environment (BPA, Phthalates, pesticides).  Conventional wisdom says diabetes is caused by eating too much.  Doctors say diabetes is caused by eating sugar.  I say who the fuck knows.

My plan going forward is as follows:

1.  Exercise.  Some form of exercise every day.  Guess I’ll be taking a lot of cold walks this winter.

2.  Blood sugar testing.  This morning I had 4oz of orange juice and 2 eggs cooked in coconut oil for breakfast.  An hour later my blood sugar was 133.  Ms. Ruhl says ideally you want it below 140 at the one-hour mark, so that qualified.  I’ll keep testing different things to see what I can get away with.  I don’t want to damage myself by subjecting myself to high blood sugars for hours and hours every day…so I’ll be testing conservatively.  This may look low-carbish at first, but only until I can increase glucose tolerance.

3.  No more PUFAs for me.  I don’t know how anyone eats healthfully without spending a ton of money.  It pains me to review our finances and see how much we spend now on groceries…and that’s with chicken and fish still in the mix.  Oh well.  It’s probably cheaper than losing a foot or something.

And on that cheerful note, good night.