Without Your Health….

…you’ve got nothing.

At the age of 44, my health is now starting to interfere with everything I care about.

This used to be a hobby…something fun and interesting to do in my spare time.  AROUND my other real-life activities like work, family, exercise…

Now my health is making all of that much harder.

I had a really good opportunity to promote my business today.  Things came up and got in the way, as things are prone to do in life.  If my health were good I could have made it work anyway.  It wouldn’t have been easy, but I could have managed it.  I would have needed a lot of energy and focus, neither of which I have right now because of my new blood pressure medication, which is making me foggy, lifeless, and depressed.

I started on one medication on Monday….a calcium channel blocker called Diltiazem.  My ankles started swelling and it did nothing for my blood pressure.  I called the doc to inform her and she told me to stop taking that one and start taking Metoprolol, a beta blocker.  Now I’m 3 days into this one and the side effects are worse – I felt like a zombie last night.  Plus my ankles seem to be swelling again, but I can’t tell if that’s psychosomatic.  And, as if that’s not enough, it doesn’t work.  Blood pressure is unchanged.  I’ve just taken one more dose – if things aren’t somewhat improved in some respect by this afternoon I’ll be calling the doc again.

I wonder how many people lurking and reading this blog are laughing and saying, “Yep…she poo-pooed the EMF boogeyman and now look at her.  She’s so dumb.  And now her health sucks too.”  Yeah, well I still don’t think it’s EMF.  I think it’s serotonin and I think the reason I’m struggling is because my body doesn’t tolerate starches, and they’re in EVERYTHING.  They’re in cocoa powder, supplements, caffeine tablets – even when I’ve avoided starch, I’ve still been consuming starch in these items.  I learned yesterday that bananas and dates contain a lot of serotonin.  Not sure if my catatonia-like depression last night was because of the dates I ate or because of the new medication.

Did you know even confectioner’s sugar contains starch?  That’s right…some sugar contains starch.

I’m beginning to think that ALL of my problems are related to high serotonin, and my high serotonin is related to starch intolerance.  The best I’ve ever felt in my life was when I gave up most starches (didn’t even know about the hidden ones yet) and ate sugar – finally I had energy (carbohydrates) and no starches to pull me down again.  And seriously, aside from followers of Ray Peat, who would try this?  How many people EVER IN ALL THE LAND actually eat a ton of sugar and eat no starches?  First of all, it’s friggen hard to avoid them because they’re in everything processed and even when following a whole food diet, they’re so darn delicious.  Second, EVERYONE IN ALL THE LAND says that sugar is bad.  It’s a foregone conclusion now – people don’t even feel the need to provide citations for this stuff anymore.  “Sugar is bad.”  Everyone in the room nods.  Duh, of course it is.  So I (and other Peatarians) might be the ONLY people IN THE HISTORY OF THE WORLD to know that starch intolerance is not the same as carbohydrate intolerance.

Here’s what I think most people do (and indeed, it’s what I did): They feel like crap and they’re overweight and showing early signs of chronic illness.  They hear low-carb or Paleo will cure it all – lower blood sugar, less inflammation, weight loss.  What could go wrong?  So they try low carb.  Some people are turned off by the fact that their energy is sapped within 2 days (about how long it takes a healthy person to burn through their glycogen) and give up.  Those of us persistent, determined, or desperate enough persevere, and eventually our body gives up signaling us to eat carbs and we begin living on adrenaline and cortisol.  Feels good at first!  Energy!  Plus, if you have an intolerance to some (or all) carbohydrates because of an enzyme deficiency (or gluten sensitivity/celiac, or whatever) you feel SO MUCH BETTER.  Not because low carb is the way to go but because the offending substance is gone from your diet.  Inflammation drops, Jack Kruse pats you on the back, and you keep going.  Weight’s dropping too – yay!  “Low carb FOREVAH!”  you say.

Until other things start failing.  Your TSH starts climbling, you’re cold all the time and your sleep starts to suffer.  Weight loss plateaus.  You say, “I must be eating too many carbs!  I’ll reduce them again because that’s what worked last time!”  So you cut down from 30g of carbohydrate a day to 20 or 10.  Pretty soon you eliminate vegetables and start eating weird things like animal hearts and fish heads.  You try to convert everyone you know, because you’re sure this is the path to health!  It has to be!  It worked for a while!  I must be doing it wrong now!

You get tired.  People on the interwebs say you have “Adrenal Fatigue.”  No you don’t.  You need carbohydrates.  EAT SOME HONEY ON A SPOON.  GO! DO IT NOW!  You’ll feel better.

Anyway, I did all that.  Did it for years.  Got really hardcore in 2012, eliminated every last shred of carbohydrate except for some veggies.  Got cavities in my teeth from malnutrition – first ones since I was about 8 years old.  Tired, stressed, a mess.  So I found Ray Peat – he said to eat carbs.  I ate them.  Started adding starches, sugar, whatever.  After experimenting I’m learning that for ME, sugar = feel good, starch = feel bad.  Low carb felt good, not because I was doing the right thing for my body but because I was avoiding something I was intolerant to.

I think my starch-eating experiment in May completely raised my serotonin level.  I break down and cry so easily now.  I never feel really happy, even when I avoid all starch (even the hidden ones).  I’ve been drinking black tea and matcha green tea, both of which contain theanine, which lowers serotonin, but I suspect they don’t lower the serotonin produced by the body, just the brain’s ability to receive or recognize it.  I say this because they do lift my mood a bit, but the effect wears off after an hour or two, and then I’m back in the middle of it again.

I think the only thing that will really work for me is to avoid all starches.  My new medication comes as a tablet containing starch.  Check it out:

The tablets contain the following inactive ingredients: microcrystalline cellulose, corn starch, sodium starch glycollate, colloidal silicon dioxide, sodium lauryl sulfate, talc, magnesium stearate, hypromellose, titanium dioxide, polyethylene glycol and polysorbate 80. In addition, 50 mg tablet contains D&C Red #30 Aluminium Lake and 100 mg tablet contains FD&C Blue #2 Aluminium Lake as coloring agents.

Seriously?  My white 50mg  tablet contains red dye?

I guess I’ll use one of these enzyme supplements I just got every time I take it.  I’m still considering taking cyproheptadine or some other serotonin antagonist, but I’m not sure it would be any more effective than tea, and it has a long list of adverse side effects.  Probably the best thing to do is just avoid starch, and over time maybe my serotonin will drop as my intestinal tract is given a rest.

I”m so tired of being tired and depressed.

Oh and by the way…I had a dentist appointment a couple days ago.  No new cavities.  After months of sugar and orange juice.  The dental hygienist, right after telling me that sugar and orange juice cause cavities, told me she was “prone to cavities” and had just had one filled.  I told her to try vitamin K.  She sounded excited about it.

Ray Peat, right again.

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.

Stream of Consciousness

After eating starches for a few days – some potatoes one day, a cup of brown rice pasta another day, and some homemade gluten-free bread another day, I spent the last 4 or 5 days being depressed, irritable, and tired.  I turned off the starch spigot 2 days ago, and last night I finally started to feel better.  Still have a short fuse though.

My body is sick.

I started feeling sick around December 2012 (here’s a random post from around that time, but there are many like it), when I was in the midst of a very stressful time in my life and was trying to maintain my health on a low-carb diet.  I now realize that that was just stupid.  The human body needs carbohydrates for fuel – especially when it’s stressed, as stress devours nutrients.  Low carb folks don’t realize this, however, because they do fine – great, even – for 6 months or a year, they lose weight, it’s all very rewarding.  And then at some point it catches up.  They’re cold all the time, they stop sleeping well, they become tired and their bodies stop fighting infections well.  I lurk over at Jack Kruse’s site sometimes and of the 5 or 10 long term followers still hanging out in the forums there, most are having worsening health problems.  They refuse to question the good doctor though.  They believe him when he says it’s their “zip code” that’s the problem (all of the EMF, you know), and several of them are planning out of state moves – uprooting their kids, quitting their jobs.  Because Jack Kruse said to!  They’re ignoring all information to the contrary, blaming themselves for their health problems rather than blaming the TERRIBLE ADVICE THEY’RE GETTING.

EAT SOME CARBS, DAMMIT!

It’s easy to sit and judge from outside, but I know I’ve fallen into the same trap.  I’ve gotten caught up in what someone is saying and I stop listening to the messages my body is sending.  I followed the low-carb path out of habit long after it stopped feeling good.

I was feeling great on a Peat-inspired high-carbohydrate (high-sugar) diet for a few months.  I felt happy – free of depression and anxiety for the first time…ever.  It was great.  I thought anxious was my personality.  Nope.  It wasn’t.  I know that now because I’ve seen what it’s like to not have it.  The last time I felt that way was about 2 weeks ago.  I remember watching my daughter play and having that feeling – that great feeling of “there’s nothing wrong.”  Even my bad body image takes a break during these periods of time, which last only a few hours. I look back my diet log in Cronometer and around then I was eating a high sugar, moderately low-fat diet at the time, no starches.

Well, that’s great, except my diabetes is probably causing endothelial damage as we speak…and of course then there’s the rising triglycerides/cholesterol (read: impending heart disease).

I’m on a merry go round of silly dietary stuff. I’m pretty tired of tracking what I eat. It would be worth the effort if I was seeing some improvement, but…I’m not. I’m tired of looking around and seeing nothing I can eat that isn’t in some way making me more sick (except milk….hm….all-milk diet?).  I’m avoiding going to the doctor because I think what’s next for me is 2-3 prescription medications, none of which I want to take, because it feels like I’m giving up.  I broke my body (somehow) – I should be able to fix it!  I’m intelligent and determined!

But also tired of running into brick walls.

I’ve decided to start another resistant starch experiment.  I ordered – and received – the 3 probiotic products (scroll a bit to see the “Frequently Bought Together” section) recommended by RN over at Free The Animal.  I may use Dr. BG’s 7 step fix-your-gut protocol. I don’t know if I’ll be using potato starch or not.  Pros: It’s still in my kitchen cabinet and it’s easy and tasteless.  Cons: Possible organ failure related to long-term use.  I’m at the point now where I’m willing to roll the dice on this one.  Or, maybe I’ll find a resistant starch that has a smaller granule size, thus side-stepping the organ death thing.  Don’t know.  I’m not going to do anything though, until I get my gut critters analyzed.  A year ago I ordered a sample kit from the American Gut Project, out of curiosity.  Then I moved 3 times within about 6 months and never got around to using it.  Only problem is, now I can’t find the sample kit. Guess I have some house cleaning to do today.

What else…oh, the hot flashes stopped a couple days ago.  Don’t know why they started.  Don’t know why they stopped.

/stream of consciousness.

Results and Changes

Had a lipid panel done today, about 2 weeks after my last one.  Over the past week I did the following:

  • Aimed for a 2:1 carbohydrate to protein ratio.  I found this difficult because I don’t particularly like sweet food, so I fell short some days.
  • Aimed for a 1:1 calcium to phosphorus ratio, because Ray Peat says.
  • Ate no starchy foods, getting all of my carbohydrates from sugar (fruit, honey, juice, and white sugar)
  • Maintained a lower-fat diet (averaged 59g fat/day or about 24% of total calories, on average).
  • Took niacinamide and aspirin 3x a day
  • Doubled thyroid supplement (Cynoplus, a combination T3/T4) from a very small dose -1/4 tablet (7.5mcg T3 / 30mcg T4) to two 1/4 tablets per day.

The results of today’s lipid panel:

  • Total Cholesterol: 316 (first time ever above 300).  Shouldn’t increased thyroid supplement decrease cholesterol?
  • Triglycerides: 495 (a 3% improvement. I’m not impressed.)
  • HDL Cholesterol: 30 (lowest ever)
  • LDL Cholesterol: Couldn’t be computed because Trigs were so high (this was the case last time too).

So, not great.

Here’s a handy chart showing my lipid panels over the last 2 years, along with brief notes about my diet during that time:

lipid panels

So you don’t have to turn your monitor on it’s side, here are the notes that correspond with the different testing dates:

3/27/2012 – Low Carb/Leptin Reset

11/14/2012 – Low Carb + Stress (Moved to a new state, started a new and very stressful job, was doing the Wiley Protocol and supplementing estrogen + progesterone).

6/19/2013 – Low Carb, without following any particular plan.  When I ate carbs they were in the form of starches from potatoes and rice, some vegetables, no fruit.

12/30/13 – Ray Peat, low sugar – around a 1:2 carb:protein ratio.  I was fiddling around with eating fruit, juice, and sugar but I was scared by the effect it was having on my blood sugar.  It was about this time I realized I was diabetic and was afraid of eating more carbohydrates.

4/19/14 – Ray Peat, high sugar – 2:1 carb:protein ratio – I decided to jump in with both feet and start eating more carbohydrates. When this test was done I was eating high fat (90-120g/day), high sugar (over 200g/day, some of which were starches), moderate protein (about 110-120g/day).  Pressure under my left ribcage was making me concerned that something might be wrong.

5/2/14 – Ray Peat – high sugar (2:1 carb:protein), low fat (around 25% of calories), taking niacinamide/aspirin/increased thyroid to address scary lab results.

According to this, my body (well, at least my lipid panel) responds best to a low carbohydrate diet, with minimized environmental stress.  I can tell you I didn’t feel great eating low carb after a while – I felt tired all the time, irritable.  But maybe that was because I wasn’t getting enough nutrition – I wasn’t tracking my food back then – vitamins/minerals were pretty much off the radar for me. I wasn’t eating liver or taking progesterone then.

Of course, other things were worse then.  My BUN/Creatinine ratio for example, got worse the longer I was on low carb, and improved since then.

BUN

Maybe eating too much meat is stressful on the kidneys after all?

Let’s look at thyroid:

thyroid

Seems sort of unrelated to sugar intake, actually, and more related to environmental stress. When I had the labs drawn in 12/2013 I was experimenting with resistant starch.  I think that was stressful on my body – I know it was stressful on my emotional state. So that may account for the increase in TSH last December.  I know TSH isn’t the ideal measure for thyroid function, according to many people…but Peat seems to think it’s a decent gross measure, so good enough.

And of great importance to me is my blood sugar.  Let’s see the data:

blood sugar

This is a crazy graph, right?  There was definitely an increase in fasting blood sugar when I started following Peat and adding carbohydrates to my diet, but that’s to be expected.  Anyone can have “well managed diabetes” with a low carb diet.  I wanted to actually FIX my diabetes, so I was experimenting with adding carbs back in to see what it would take to do that.  From the graph it looks like the best things I did for my blood sugar were bicycle for 30 minutes a day and eat a low-fat diet.

Holy crap!  Just like my conventional doctor told me!  Exercise and eat a low fat diet!

hahaha

It does seem my current supplements are confounding things.  The graph shows that eating a low-fat high sugar diet results in lower fasting blood sugar…but not if I add niacinamide, aspirin, and increase thyroid.  Hm…interesting.  If I was a patient person, and if I really loved sweet food, I’d probably just eliminate the supplements I’m taking and go back to high-sugar/low fat for a while to see if that trend continues.

I’m neither patient nor in love with sugar.

And considering that I’m STILL having hot flashes – even while sitting right here, right now, I’m going to stop taking niacinamide, aspirin, and thyroid.  One of them is bothering me.  Later on I may try to add them in one at a time and see what I can tolerate.

So to sum up: It looks like the best thing for my lipids is low-carb.  The best thing for my BUN/Creatinine is low meat.  The best thing for my thyroid is low-stress.  The best thing for my blood sugar is low fat and bicycling 30min a day on flat terrain.  The best thing for my enjoyment of life – to not have to eat so much sugar.  I really don’t look forward to it.

So what kind of diet is low-carb, low-meat, low-fat, and lower-sugar?  Maybe one with dairy (mostly low-fat), some lean meat, lots of vegetables, some fruit (when I feel like it).  Plus avoid stress and get exercise.

I still love Ray Peat – he gave me progesterone, Vitamin E, red lights, liver, vitamin K, dairy, raw carrots, and taught me that estrogen, PUFAs and serotonin are bad guys.  I’m continuing on with much of what he has to say.  Just less sugar.  More vegetables.  More exercise.

I might as well retire the blog.  I have nothing original to say anymore.

So there it is.  That’s my new plan.

High Carb Low Fat (HCLF) – Day 2

My stats for today:

crono2

Did better today keeping meat consumption (and thus phosphorous) low.  Calcium:Phosphorous ratio today was just under 1:1 (2095mg cal, 2161mg phos).  Had almost a 3:1 carb to protein ratio – that’s a first for me.  I’m struggling a little to eat enough sugar – I just don’t gravitate toward it the way I do to salt and meat.  I realize that marshmallows aren’t ideal food, given that white sugar contains no nutrients other than, well, sugar for energy.  It’s an easy food to take with me when I go out though, and it’s a nice combo of carbohydrates and gelatin with almost no fat.  Fat was a little higher than ideal today at 23% of total calories consumed, but still pretty low.

HSLFDE – Day 5 (Updated)

Blood sugar this morning was 117.  That’s the 3rd day in a row with a fasting blood sugar under 120.  The last time I had 3 days under 120 was November – 5 months ago – when I was still essentially eating low-carb and cortisol was getting me through the day (poorly).  I do think that eating very little in the way of carbs late in the day yesterday led to increased stress hormones overnight, and thus a rise in sugar level today.  But still.  Under 120.

Update 10:11PM:

Cronometer had this to say about today:

  • Calories: 1507
  • Protein: 141.2g (39.5%)
  • Carbs: 138.1g (35%)
  • Fat:43.5g (25.5%)

My GI system is still a mess so I really just ate what sounded good.  Still low fat though.  Just not as many carbs or calories as I’d normally eat.

On another note – Here’s a site worth checking out if you’re looking to lose weight…and the information is free. Sean Bissell participates in one of the Ray Peat Facebook groups and may have cracked the weight loss code that we’re all looking for.  I may be trying out his system after the current experiment.

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.

Sugar: Not Just For Breakfast Anymore

I’m really struggling to eat Peat-ish and remain low fat.

I’ve given up starches because they were making me feel depressed.

I’ve given up eating lots of meat because it’s high in phosphorous.

I’ve given up alcohol because it made me depressed.

And now I’m reducing fat.

I’m trying to determine whether it’s all fat (not just PUFA) that blocks cells from using available glucose, keeping blood sugar high.  My blood sugar has come down over the past week of lower-fat eating, but I’ve also completely given up starches at the same time.  I’m trying to avoid changing more than one thing at a time, but the starches had to go.  They were really messing with my mood.  In the past when I gave up starches but kept fat intake (and sugar intake) high my fasting blood sugar would reduce from really high (140-150) down to the 120s, and that’s what it’s done again this week.  I’d like to continue my low-fat eating for a while and see if it improves further.

Now about that…You know what’s left when you give up starches, most meat, and fat?

Sugar. Currently 200-250g of it.  And maybe some vegetables, and some lean meat. Just a whole lotta sugary sweet stuff – fruit and fruit juice, milk, honey-sweetened coffee, marshmallows.  Anything to keep me from being hungry and also not add to the dietary fat total. If I have a couple ounces of cheese and 2 eggs per day I’ve about maxed out my allowed fat intake.

I don’t even really like sweet stuff.  I’ve never had much of a sweet tooth, and now my diet is centered around it.  Day to day I’m feeling pretty good, but I fear this is unsustainable because I just don’t really like it.  I’m coming to dread my next sugary coffee/milk/orange juice.  I know low-fat cheese is an option, but even that has 4g of fat per ounce.   I’ve identified one brand that doesn’t have much in the way of unwanted fillers.

Anyway, my weight is down a pound this week…I guess that’s good, and I hope it continues.

I’ve been tracking what I eat on Cronometer.  I don’t know what my baseline (maintenance) number of calories of fat grams is – I haven’t tracked that – but considering how I feel when I restrict calories/fat, I suspect I was maintaining my current weight on 2500-3000 calories per day and over 95-100g fat. A few weeks ago I was trying very hard to lower overall calories without making an effort to reduce fat, and I was averaging 1807 calories and 83g of fat per day.  Hunger was (and still is) preventing me from going lower.  This past week I averaged 1966 calories per day and 58g fat per day, and it was a struggle for the above mentioned reasons. The totals for the last 2 days of the week skewed the average because I was starting to tire of all the sweet food. I think I’ll try to stay under 50g of fat per day – that would be challenging but maybe not unrealistic.

Otherwise, I’m meeting all of my micronutrient goals, and my phosphorous/calcium ratio is about 1:1.  It’s really just a matter of being bored with the taste of sweet.

Onward.

Low Cal – Day 2

So, I’m shooting for 1700 calories per day in an effort to lose weight.

Yesterday:

  • 1911 calories
  • 128g protein (19%)
  • 92g carbs (28%)
  • 115g fat (53%)

Well, a couple of comments about this.  Clearly, I still tend to automatically go for high protein/fat when I’m hungry.  Probably in part because that’s what I’ve done for years, but also because they kill my hunger (And my motivation to live. But I digress.).  Ray Peat sometimes refers to the “Randle cycle” which is a phenomenon in which glucose oxidation is inhibited by fat.  He says this is what ACTUALLY causes type-II diabetes – not sugar.  Oh sweet lawd…NOT SUGAR!  (An aside: Fer crissakes…if I see one more reference to this study this week I’m going to throw my computer out the window. Newsflash!  Eating Poptarts and Mountain Dew isn’t good for you!  How about this for scientific integrity: Isolate your independent variable, dumbasses.  Oh geez…I think I’ve been reading too much Richard Nikoley.  I’m starting to talk like him.)

Anyway, where was I?  Oh yeah, the Randle cycle.  I was reading up on this today, after seeing all the fat I’m still consuming (almost all of which is saturated), and found this little nugget by Dr. Peat:

The antagonism between fat and sugar that Randle described can involve the suppression of sugar oxidation when the concentration of fats in the bloodstream is increased by eating fatty food, or by releasing fats from the tissues by lipolysis, but it can also involve the suppression of fat oxidation by inhibiting the release of fatty acids from the tissues, when a sufficient amount of sugar is eaten.

Huh…I’ve heard him say that PUFAs can block the cells from using available glucose and that FFAs released by the body can do the same, but I didn’t know good fats in your diet could inhibit glucose oxidation too.  Hm….Well this changes things. I mean, my fasting blood sugar is still in the 120s most days, and not showing much improvement since I’ve given up most dietary PUFAs.  OK then – Time to go on a Peat-friendly low-fat diet.

So here are today’s Cronometer stats:

  • Calories: 2027
  • Protein: 130g (26%)
  • Carbs: 210g (40%)
  • Fat: 77g (34%)

Hm…well, that’s better than the previous day, but clearly this is going to take some tinkering.  I got really hungry – like mean-hungry, desperate-hungry…eat pasta hungry (didn’t, but wanted to).  I don’t know how to cut these calories without hunger.  I guess maybe, like everything else, this is going to be a process…and it’ll take time.

And here’s another psychological challenge that’s in the works for me.  I’ve managed to give up starches (6 days now) but how I manage to keep from being hungry is sipping on honey-sweetened coffee or orange juice throughout the day.  I’m becoming concerned about the effect of sugar on my teeth.  I understand it’s not just the tooth’s exposure to sugar that causes cavities – it’s also nutritional status, the presence of specific kinds of bacteria in the mouth and other variables.  I think this paper does a nice job of describing the pathology behind tooth decay.  I’ve been rinsing my mouth periodically with water/baking soda as Peat recommends, but this is still on my mind a lot.  I really don’t want a mouth full of bad teeth.

Anyway…till next time.

Good Times

I’ll get to the resistant starch stuff…later.  That’s going to take a little research and a little discussion that I’m too tired to articulate right now.  But we’ll get there.

Today, just for a minute, I want to talk about how much better I feel now than I did 2 months ago.  Two people in my life this week commented to me that I’m not moody or depressed anymore.  One of those people has asked me for help with his mood problems. I gave him a Ray Peat-inspired shopping list and told him to buy some lights.

I few months ago when I started following Peat’s recommendations I never felt at peace.  I realize this now only because now I have stretches of time that I feel GREAT.  Like, peaceful and happy and content with my life exactly as it is.  A complete lack of anxiety or depression.  Back in November I started having these moments.  They were fleeting, but they were there.  Just in the last week or so those moments have been lasting longer – for hours sometimes!  I have no idea what is happening biochemically in me that causes that feeling, but it’s fabulous.

This week I got my period and had no PMS.  Well, that’s not entirely true.  I had a mood swing that lasted all of 5 minutes which made me cry for no good reason.  That was it.  My PMS used to last days.  DAYS.  And now it’s over in 5 minutes.

Also, this week, my hunger stopped being so crazy.  I feel like a normal person again, and have for the last 5 or 6 days.  No crazy appetite.  WTH?

I’ve got the whole family on the Peat plan now.  I make Peat-friendly meals and we all eat them.  My daughter used to get rashes when she drank milk.  She would get them around her mouth and in random areas on her body.  She also used to have keratosis pilaris (KP) on her arms and cheeks. Turns out that milk doesn’t CAUSE these skin problems…milk causes an increase in nutrient metabolism, requiring more vitamin A.  The deficiency of vitamin A causes skin problems.  Now she gets plenty of vitamin A in her diet and no longer has rashes or KP.  Brilliant!  Thanks for making that clear, Dr. Peat.

Anyway Peat offers no quick fix, no express train to a lean body.  But if your goal is to be happy and to feel at peace, even while carrying those extra pounds, this (for me, anyway) is the way to do it.