New Plan 3.0

I’ve been eating starches for almost 2 week now, and they make me feel like taking a nap. Every time.  Some of the common reasons folks get tired in the middle of the day are sleep deprivation, lowering of stress hormones, and food intolerance.  Hm…There’s no way I’m this sleep deprived.  There’s no way my stress hormones are super-high and the starches are lowering them, thus revealing my “true fatigue” (cuz if that were the case, sugar would have made me sleepy too). There’s no way I’m intolerant of every kind of starch…is there?  Is it possible white potatoes, sweet potatoes, rice, oatmeal, and gluten free bread/pasta are all making me tired because my body is completely intolerant to all of those foods?  No.

I don’t know why this is happening, but it sucks.  I can handle about 1/4 cup of potatoes with a meal before I get too tired to function.  And even then I don’t have much energy.

So my conclusion – for now – is that I won’t find the solution to these problems in my diet…because EVERYTHING (with the exception of maybe milk and dill pickles) seems to be killing me or killing my enjoyment of life.  Or both.

So here’s my new plan:

I’m going to focus instead on exercise.  The last time I got in the habit of bicycling every day my blood sugar improved dramatically, dropping to within normal ranges within a week. I stopped because it got cold outside and because I was afraid my slowing pulse meant my thyroid wasn’t happy.  Things are more dire now….because now I have diabetes, for realz. Uncontrolled diabetes.  A couple days ago my fasting blood sugar was 155 – not an all time personal record or anything, but too flippin high.  When I first started eating starches my fasting blood sugar dropped to between 110 and 120 for a few days (don’t know why) – now it’s above 130 every day.

Yesterday I started biking.  I biked today too, and will tomorrow.  And the next day.

So what to eat?  For now, mostly Peat-friendly foods, without much of a plan. Someone on Facebook linked to this interesting study about saturated fats causing greater insulin resistance than monounsaturated fats.  They found that among people who ate less fat than the median (I think it’s less than 37% of calories, but I’m not sure and don’t have the full-text of the study), monounsaturated fats (e.g., olive oil) promoted insulin sensitivity, while saturated fats caused greater insulin resistance.  Can’t say I’ve ever heard that before.  I do eat about 40% of my calories in the form of saturated fats right now, so it may be a good idea to try substituting some olive oil, and reduce fat overall.  So that’s what I’m going to do. I’m not going to be crazy about it, but I’ll stop adding fat when its not necessary, and swap out some of the saturated fat for a while.  Olive oil has more PUFA than either butter or coconut oil, but that’s just going to have to be ok.  For now.

I predict my fasting blood sugar will be in the 90s within 2 weeks.

My resistant starch + probiotics experiment continues.  I’m so scared to up my potato starch intake because of the extreme GI distress it caused me before.  But I must.  Maybe tomorrow.

If my blood sugar isn’t under control within 1 month, I’m going to see a doctor and get medication.  I feel like my time to noodle around has run out.

I’m so tired from eating starches – even just 1/2 cup of potatoes or rice – 15g of carbohydrate – that I find myself avoiding them.  Low carb is no good for my thyroid.  High sugar no good for my triglycerides.  Out of time, out of ideas.  If exercise and olive oil don’t fix this very soon I’ll have to give in.

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 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.

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.

Labs

So here are the lab results I’ve received so far:

Test Me Range
T3 Uptake 32 24-39
T4 7.9 4.5 – 12.0
Free T4 0.94 0.76 ‑ 1.46
Free Thyroxine Index 2.5 1.2 – 4.9
TSH 1.68 0.358 ‑ 3.74
Cortisol 12.8 2.3 – 19.4
TPO 8 0-34
Antithyroglobulin Ab <20 0-40
Glucose 98 65-99
Cholesterol, Total 222 100-199
Triglicerides 107 0-149
LDL Cholesterol 147 0-99
HDL Cholesterol 54 >39
Vitamin D 34.2 30-100
HS C-Reactive Protein 8.65 0-3.00

So I’m obviously no expert when it comes to interpreting this stuff, and I only have about 10 minutes before I have to go to work.  But here’s what I’ve surmised so far:

My thyroid appears to be functioning normally.  The TPO and Antithyroglobulin Ab test indicate that I test negative for Hashimoto’s or other autoimmune thyroid problems. Since my thyroid seems to be ok, I’m guessing it’s stress/adrenal fatigue/high cortisol causing the hypothyroid symptoms I have.  I’m still waiting for my hormone panel, including 4x/day cortisol testing.  Hopefully that will show up soon.

My total cholesterol has improved since it was last tested 2 weeks prior (no…I don’t plan on testing my cholesterol every 2 weeks…it just worked out that way!).  But seriously, it dropped from 238 to 222 in 14 days of eating meat and fat!  My LDL dropped from 165 to 147.  That’s an 11% drop in the “bad” cholesterol in 2 weeks!  HDL is up a bit too.

I love knowing the truth about saturated fat!

Ok, but that’s where the good news ends.

Vitamin D is on the very low end of normal, and that’s with supplementing about 3000 IU/day for the last month or so.  I’ll be upping it to 10K units.

And the worst news…my HS CRP – 8.65.  That’s some serious inflammation!  Anything over 3.00 is highly correlated with heart disease.  I guess I’m about to keel over from a coronary right now!  I wish I had a baseline from before I started the Leptin Rx…this might actually represent an improvement from where I started.  I know other markers of inflammation are coming down (blood sugar, cholesterol), so this may have been really out of control 2 months ago.  In any case, I need to get that number down.  I’ll be continuing to address possible leaky gut issues and increase Omega 3 and seafood.

Would like to stay here and talk about my blood all day.  Must go to work.

Leptin Rx: Week 4, Day 5

I feel like I have a lot to say today.  Maybe I just have a lot of energy so I’m feeling chatty.  I think it’s interesting that when I was just eating low-carb I felt tired all the time and had all kinds of cravings.  Here are the difference as I see them between my low-carb lifestyle (a la Atkins) and now:

  • Low Carb:  I ate something early in the morning but was usually hungry again by 9:30AM or so.  I don’t think I was eating enough.
  • Now: I’m eating as soon as I wake up, between 50 and 75g of protein.  I start getting hungry about 6 hours after eating breakfast. If I can’t eat right away though, it’s no big deal.  I can put off hunger for 1-2 hours by drinking water.
  • Low Carb: I was also kind of eating low fat.  I still believed animal fat was evil, so I was eating a lot of low-fat boneless skinless chicken breast.  I was worried that saturated fat caused heart disease, so I went easy on the butter too.
  • Now: I’m actually adding fat to my green tea.  It’s insanity!
  • Low Carb: No tropical oils.  Saturated fat was evil.
  • Now: I’m downing coconut oil and Nutiva’s Coconut Manna at an amazing clip.  I calculated I consume about 3 oz per day of the manna, and 2-3 Tbs a day of coconut oil.  Yay for healthy and nutritious saturated fat!
  • Low Carb: I was snacking all the time.
  • Now: No snacks. 3 meals. Period.
  • Low Carb: I was tired all the time.  I came home from work and wanted to sleep.
  • Now: I have a ton of energy.  I wish I had more waking hours to do all the things that are interesting to me right now.  I have to prioritize.
  • Low Carb: I drank cans of diet soda or coffee with sugar-free sweetener throughout the day.  I didn’t like drinking water.  I needed a lot of caffeine to stay awake and alert.
  • Now: I have 1/2 of a caffeine pill in the morning (100mg), and maybe some green tea in the afternoon.  I sometimes forget the caffeine pill and I’m fine.  I do still like caffeine though, and feel a little better if I take it.
  • Low Carb: With all the caffeine in me from the diet pop, I usually didn’t feel like going to bed until 11 or 12…and I was losing sleep all week because of it.  My mood was foul a lot of the time.
  • Now: I go to bed when I’m tired, usually around 9:30 or 10:00.  I miss the time I had to myself when I stayed up late, but I do feel better throughout the day, not being so sleep-deprived.
  • Low Carb: Lots of cheese
  • Now: About 1oz of cheese 3-4 times of week.  Otherwise no dairy.
  • Low Carb: Lots of nightshades
  • Now: Very few nightshades…maybe 1-2 oz of chopped tomatoes that show up on a salad at a restaurant 1x a week.  Dr. K. says nightshades cause a leaky gut.  I have a personal problem with the term “leaky gut.”  Why don’t they call it “leaky intestine” or “leaky colon.”  Then maybe it wouldn’t sound so “woo” like.

I do have much more energy now.  I now come home from work and have the energy to play with my daughter – for 2 hours sometimes – whereas I used to need a nap or a long break from social interaction.

Mood.  My husband and I were just talking about changes he’s seen in me since I stared eating a Paleo diet and following the Leptin Reset.  He said to me, “You have no idea how crazy you were.”  Apparently my mood swings were fairly extreme.  I don’t remember it that way, but…well, he’s probably right.  And I was taking antidepressants then.  Now I’m off of the meds and feeling positive every day.