Labs

Some updated labs this week.  First, some background information, for those not following along….In February 2015 I adopted a low carb Paleo diet as well as lots of supplements recommended by my advisers at Nourish Balance Thrive.  I felt great for a while but after a while started to have a lot of sugar cravings and my hair began falling out at an accelerated rate.  I also started feeling tired and stopped losing weight.  In September I started eating carbs again, and in the middle of December (about 10 days prior to these labs) I dropped fat way down to about 25g/day and kept carbs high at about 250-300g/day.

So how are things going?

Let’s take a look at the basic metabolic panel first (click to enlarge):

Metabolic Panel

Notable items:

  • HbA1C: 6.4 (high)
  • BUN/Creatinine Ratio 28 (high, but improved)
  • Carbon Dioxide – 28 (much improved)
  • ALT (liver enzymes) – 39 (worse)

Fasting blood sugar somewhat improved (honestly I’m happy if it’s under 110).  HbA1C would have been in the 5’s if I would have tested it during low carb, but currently it’s high (6.4).  Considering that it reflects an average blood sugar over the last 3 months I’m not surprised by this.  During one of the last 3 months I was eating relatively high fat and high carb and the same time and my blood sugars were trending up.  This was improving over the last several weeks when I eliminated most fat.  Still, it’s not good and is still in the diabetic range.   BUN/Creatinine ratio tends to go up when I’m eating a lot of meat, and meat has been my biggest source of protein these days.  CO2 – better, and important in Peat world.  ALT – worse.  Fatty liver caused by….the tablespoon of honey I’ve been putting in my tea?  The tablespoon of sugar I’m sprinkling over out-of-season berries?  High carbs?  Dunno.

Next – Lipid Panel:

Lipid Panel

AAAAAAaaaand here’s where we run into some more serious trouble:

Notable elements: everything.

Cholesterol still high but much improved over my low-carb labs.  Triglycerides.  Seriously?  Look that that monster.  477.  I haven’t been eating that much sugar – most of my carbs come from white rice.  So I’m pretty confused at this point what is actually causing my trigs to be that high.  I know sugar can do that but I didn’t know glucose did that.  Any biochemists out there care to enlighten me?  With high triglycerides seems to come a dropping of HDL cholesterol and imminent death.  If I don’t come back you’ll know why.

And finally, thyroid.  I only had TSH tested because that’s all my doc would order and thus all my insurance would pay for:

Thyroid

Hey look – my TSH is the best ever in the history of me.  Thank you for that, carbs.

So to summarize, I can’t continue on this way.  I eat low carb high fat and my thyroid suffers.  I eat high carb, low fat and my triglycerides skyrocket. High fat/high carb and I’ve got blood sugar problems.  High fiber causes depression via endotoxin poisoning (see here and here for just two of the many examples of this).

Perhaps the answer isn’t in my diet.

My doc called me the morning after these labs were processed and told me she wanted to make an appointment to discuss my labs. I feel like I’ve been called to the principal’s office.  My appointment is later today. I’m sure she’ll be pushing the Lipitor and the Metformin.  I’ve been giving a lot of thought over the last few days as to how I’ll be handling this.  I think what I’m going to do is start exercising daily and stop thinking so much about food.  I’ll do the best I can to follow a nutrient dense diet and let the macros take care of themselves – probably fewer carbs early in the day and more later in the day – while getting at least 45 minutes per day of exercise – a combination of walking/cardio and strength training.

I know the first week or two is the hardest.  I was an athlete the first half of my life, and a gym rat until about 8 years ago.  I just need to get over the initial resistance until it starts feeling good again.  No nazi trainers this time.  I’m just going to do it.

I’ve been phasing out the supplements I’ve been taking, and making more of an effort to get nutrition through food.  I’ll be continuing this.

My personal life is still a bit of a mess, but things are stable at the moment.  Stable enough to start taking better care of myself and start remembering who I am and what I’ve given up over the years.

Plan of Attack

I’m very much back on track now…inspired by my last set of not-so-hot labs.

My short term goals are as follows:

Maintain a higher-carb, lower-fat diet in order to reverse my type 2 diabetes and reverse my abysmal lipid panel.  Rationale:

  • Lower fat to address high blood sugar (<20% of total calories, or in the neighborhood of 40-50g/day).  My dabbling in low-fat eating in the past month or two suggests that Ray Peat may be on to something when he talks about the Randle Cycle.  He says glucose oxidation is impaired by a high fat diet and/or fatty acids in the blood stream.
  • Higher carb in order to reduce stress hormones (namely, cortisol) (>250g carbohydrate) – Nearly all in the form of simple sugars – no starches, as those make me depressed, with the goal of eating at least a 2:1 carbohydrate:protein ratio.
  • High calcium intake (nonfat dairy, most likely), low phosphate intake (less meat).  I’m going to shoot for a 1:1 calcium:phosphate ratio.
  • I’m not going to make any effort to restrict calories.  That’s stressful and no fun.

Change my supplement routine to include the following:

  • Aspirin 100mg 3x/day
  • Niacinamide 100mg 3x/day
  • Vitamin K2 1mg 3x/day
  • Cynoplus (T3/T4 combo) increased from 1/4 tab daily to 1/4 tab 2x a day.  I may increase further in a few weeks, but that’s it for now.

The aspirin reduces inflammation.  Niacinamide inhibits the release of free fatty acids into the blood, and vitamin k2 ensures that blood clots normally despite the aspirin, and that calcium goes into the bones rather than the soft tissues.  Cynomel provides thyroid hormone that I don’t seem to be making enough of (evidence: total cholesterol of almost 300).  I’ll continue to take Vit D (5000 IU), Vitamin A (2500 IU), and Magnesium Glycinate.

Knowing that I have a tendency toward poor planning and then eating whatever’s available, I’m going to create some accountability for myself with this blog.  I’m going to post a screenshot of what I enter into Cronometer every day.  Here’s today:

Crono1

This will make it difficult for me to rationalize eating things that don’t support my goals.  Also it’ll force me to take a critical look at what I’m eating each day so I can learn from it and do better.  Today, still too much meat…instead of chicken breast I should have had more dairy or something with gelatin in it.  At the time I just wanted to stop feeling hungry – a big dose of meat does that well.  Time to learn new strategies.

Macro % today:

  • Protein: 30.9%
  • Carbs: 50.4%
  • Fat: 18.6%

More to report tomorrow.

Getting Back on Track…and New Labs

I was wrong…my HSLFDE was not resumed…It’s still paused.  I’ve been having a hard time getting back on track.  One day of bad planning and I’m eating crap food from a restaurant…then visiting people and eating their crap food…then another day of bad planning….you get the idea.  I’m still tracking what I eat so it’ll all be data for my experiment, but I do want to get back on track with the intervention portion of the experiment – I think I’ve got a pretty solid baseline at this point, from which to measure.

It looks like in 16 days a movie will be hitting theaters called Fed Up: “…the film the food industry doesn’t want you to see.”  Hm…well, that has potential, right?  But then I scroll down and see there’s a “Fed Up Challenge” – can you be “sugar free for 10 days”?  Like that’s the ticket to awesome health.  Yeah, I can be sugar free for 6 months.  You know what that gets me?  High cortisol, high BUN/Creatinine, high TSH, low energy, low mood, low interest in interacting with my child….shall I go on?  So yeah, great…more anti-sugar propaganda.  Makes me even more determined to stick to a low-fat Peat-inspired diet for a while, so I have some N=1 data to point to when this movie starts making waves.

Got some lab results today.  Numbers are fun.
labs1
labs2labs3

Current labs are in RED.  If there’s a space with no result, that means I didn’t get that test done this time.  Money is always an issue with labs…I try to get just what I need to track progress.

A couple thoughts about these…Let’s start with the good stuff.  My BUN/Creatinine ratio is coming down.  It reached it’s peak of 34 when I was eating low carb and under a lot of stress.  It’s come down gradually and is just a little over the range now.  I’m not sure what this is about – I know BUN and Creatinine have to do with kidney function and can indicate dehydration.  I guess I drink more fluids now but don’t drink much water these days…too much to drink with actual nutritional value, like milk, juice, or coffee.  Or maybe the improvement is because I’m not eating as much meat as I used to?  Less work for the kidneys?  Anyway, nice to see improvement there. Calcium Dioxide is now 21 instead of 20…a very small improvement.  Maybe that’s from the addition of carbonated water to my diet?  I mix a few ounces with OJ in the morning – it’s so awesome that way.  I should really start bag breathing and get that CO2 level up. Thyroid function may be improving – TSH is down from last time.

OK, that’s it for the good stuff…now, seriously.  512 for triglycerides?  That’s kind of high.  Like 10 times higher than I want it.  Conventional wisdom says that high triglycerides are caused by eating too many carbohydrates.  Hm…maybe.  I asked the smarties on my Ray Peat Facebook page for input and got the following responses:

Niacinamide 3x a day. Too much cortisol. Coconut oil. get enough calcium and reduce phophates.

and

This was from a kmud interview, mar 2014 – “niacinamide inhibits the lipase enzyme which liberates the free fatty acid’s from the triglyceride stores in the tissue. aspirin also does this.”

These comments are from people I’ve come to trust, so I’ll give niacinamide a try again.  I stopped it because it didn’t seem to be making a difference in any way I could sense.  It would be worth it though to bring these numbers down.  Also, the  “too much cortisol” and “reduce phosphates” comments hit home – I still eat too much meat.  I need to embrace carbohydrates and stop eating so much meat.  Darn the carbophobia.  Right now my carbohydrate:protein ratio is about 1:1.  I need to pretty much double my carbs and cut my protein by 1/3 or so.

They couldn’t calculate my LDL cholesterol because my trigs were so high.  Can you believe that?  I’ve never heard of that.  I’m off the charts.

Looks like MCHC was a little low.  I don’t know what that means, but Google says I might be a little anemic.

That’s about it.  Please feel free to analyze and share your interpretations of these numbers.

Also please feel free to feel superior to me because my labs suck, and link to my blog from your blog and talk about how you’ve got it all figured out and about how much of a loser I am to be continuing on my current path.  Go ahead.  It’ll be fun for everyone!

Just kidding.

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.

High Sugar Low Fat Diabetes Experiment – Day 3

Day 3 of the HSLFDE.

I have to say, I’ve been feeling really good the last 2 days.  Like, in the happy zone for a large proportion of each day.  Not sure what to attribute that to, except maybe eating more sugar than I was previously.

Also – get this – my fasting blood sugar was 113 this morning.  That’s the lowest it’s been…since March 3rd – a full month.  And before that it was a couple months.  That’s how rare it is to be under 120.  And…get this…down a couple pounds on the scale this morning.  I’m probably jinxing it by telling you this, but jinx be damned!  What do I attribute this to?  Glycogen stores being filled (or closer to filled) due to higher sugar intake could result in lower fasting blood glucose.  Not sure why I’ve dropped a couple pounds – perhaps this is a correction from the 2 pounds I’ve gained over the  past couple of weeks (wasn’t sure why I gained, not sure why I’ve lost).  In any case, we’re talking one data point – nowhere near a trend.  But still…it gives me hope.

The last 2 days my macros were as follows, according to Cronometer:

4/3/14 (yesterday):

  • Calories – 2158
  • Protein – 153.8 (29.9%)
  • Carbs – 283.2 (50.2%)
  • Fat – 48.4 (19.8%)

So a little higher in the fat department than the previous day….maybe 15% isn’t realistic.  Again, I’m not restricting calories in any way.  If I’m hungry, I eat.

4/4/14 (today):

  • Calories – 2247
  • Protein – 190.2 (35.7%)
  • Carbs – 271.4 (46.4%)
  • Fat – 45.6 (18%)

Ate a lot of meat today – too much.  Must embrace the gelatin.  It’s a struggle for me I suppose not just because I’ve been turned off by the taste but because I don’t get as much salt as I used to now that I’m eating no starches and eating more sugar…and meat + salt = perfect.  Bear with me – my entire transformation from low-carb to Peat has been one step at a time – no big moves – two steps forward, one step back.  My acceptance of it has been gradual…but I’m coming up on 6 months of Peating now.

Will update with more numbers tomorrow.

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.

Low Fat – 2 Week Review

A couple weeks ago I decided I was going to change one thing at a time and stop confounding all of my variables, so I have a shot at actually knowing what is and what is not helping me.  I decided to start with eating low-fat, which Ray Peat says should help with weight reduction. But more importantly, I wanted to test to see if fat intake would have an effect on my blood sugar.  Most people (and doctors) believe diabetes is caused by eating too much sugar.  Peat says otherwise – that the cells’ uptake of glucose is impaired by fat intake.

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.

I have previously interpreted this as being primarily polyunsaturated fat being the problem, and reduced my PUFA intake…but my blood sugar stayed disappointingly high.  A re-read indicates he doesn’t actually doesn’t say PUFAs alone are the culprit – he says that dietary fat (doesn’t specify which kind) competes with sugar to get into the cells and provide energy.  High fat = poor glucose metabolism.  Well, I’ve had a high fat diet for the last 2-3 years, and also have had increasingly poor glucose metabolism.  So I thought I’d try to reduce fat in my food and track my fasting blood sugar to evaluate for effect.

So I started eating low-fat on 3/18/14 – not quite 2 weeks ago.  I stopped for 5 days in the middle of my experiment because I was tired of eating sugar all day long.  I don’t even like sugar.  When you don’t eat starches (I don’t…makes me depressed) and you’re limiting meat and fat, you end up eating a lot of sugar (fruit/juice/honey) for fuel.  I think Peat would say that’s ideal, but I was getting tired of eating so much sweet stuff.  So I gave up in the middle. When I did that, though, I noticed an interesting blood-sugar trend.  So I again went low-fat for a few more days to see what would happen.  Here are the results:

Blood Sugar vs Fat Intake

My blood sugar is high.  I’m pretty much diabetic.  This is a given.  But look at what happens when I reduce the fat in my diet, increase it again, and then reduce it again.  By starting and stopping I managed to create a reversal experiment.  The graph shows a decent correlation between fat intake and fasting blood sugar.  When I eat more fat my blood sugar goes up – less fat, and it goes down.

Now take a look at what happens when I add my carbohydrates intake to the graph – remember this is all simple sugars.  I’ve eaten no starches over the past 2 weeks.

add carb

Because I have to eat something, generally less fat = more carbohydrate intake.  Overall though, carb intake was pretty stable – and it appears to be completely unrelated to my up-and-down fasting blood sugar.

What do I conclude from this?  Well, it’s hard to draw firm conclusions given the short duration of the experiment, but it sure looks like high blood sugar (and possibly type-II diabetes) are related to fat intake much more so than to sugar intake.

RAY PEAT – RIGHT AGAIN!

So what am I going to do about this?  Actually, it’s almost nice enough outside to get out on my bike again, and I intend to do that.  Biking for 30 minutes a day on flat terrain at moderate intensity has reliably lowered my blood sugar in the past, and I really like it.  So that’s what I’ll be doing about my blood sugar.  Low-fat just isn’t working for me.  I quit it twice in 2 weeks because it was making me feel all eating-disordy.  Like, feeling resentful and deprived and fantasizing about bread.  I think it could be done if someone (unlike me) could tolerate starches well, but this just wasn’t working for me.

So diet-wise I’m back to eating a regular Peat-y diet – I’ll try to find a balance with fat where I’m eating less than I have in the past but not so little that I’m afraid of a teaspoon of coconut oil.  Probably somewhere in the neighborhood of 70-80g per day.  I’m also done tracking what I eat for a little while.  It’s easy to get obsessed with this stuff.  In a bad way.  I don’t want what I eat to be so damn important.

So what experiment am I going to try next?  I really want to add 10mg of B6 to my supplement regimen, to better help with estrogen management, reduce serotonin, and help with libido.  Will start that today and will report back in 2 weeks.