High Carb Low Fat – Day 8

Fasting blood sugar this morning: 117.  Nice to be below 120 again.  I’m not sure why but I have assigned 120 some sort of significance in my mind…I guess I was “prediabetic” for years and my blood sugars fluctuated between 100 and 120 – so when my fasting blood sugar is under 120 now it feels like I undid some damage.  I’m sure this is magical thinking.

Weight has been stable for the last 5 days at exactly 207.5.  I don’t know why, but since I started following the recommendations of Ray Peat my weight is exactly the same every day unless I eat starches…no ups and downs because of fluid retention.  Maybe it’s because I eat gobs of salt now and my body feels no need to retain water anymore.

Thermoregulation is still off.  Not as many hot flashes today, but still having them.  I wonder if it’s completely unrelated to niacinamide.  Maybe I’m in menopause!  All of a sudden!

Here are my macros today:

crono

Too much protein, but I just felt like eating meat today.  So I did…but it messed up my carb:protein ratio.  Fat % was good today at 21%, calcium-phosphorus ratio was shy of 1:1 by about 200mg calcium.  Overall, pretty good day.

So now, to avoid unwanted additives, I’m using bulk aspirin powder and niacinamide powder 3x a day.  I’m not sure how other people do this without feeling burdened by it…I mean, do they bring their little milligram scale to work with them and measure out their teeny tiny quantities of bulk supplements on their lunch break?  Definitely not as convenient as tablets.  Well, I came up with my own method so I only have to measure and dose once, first thing in the morning, and I can pair it with other nutritious food.  First, I get coffee brewing.  While I’m doing that I get out my little milligram scale and 3 pint-sized jars.  My coffee maker makes 24 ounces of coffee (it’s little). (Note: I make weak coffee so in my nutritional breakdown, above, I only record 12 ounces, even though I drink 24 ounces of coffee). 

Ok, so I get a bowl out.  I pour all 24 oz of coffee into the bowl, and add 3 tablespoons of honey and a heaping 1/2 teaspoon of salt to the coffee, and stir until dissolved.  Then I fill each of the jars half way with the coffee mixture. Then I measure out my aspirin and niacinamide and add them to each of the 3 jars, as well as a drop of Vitamin K2.  So now each jar contains 8oz of coffee, 1T honey, 1/6 t. salt, 100mg aspirin powder, 100mg niacinamide powder and 1mg K2.  Then I fill each jar up with skim milk.  Finally I put lids on each jar and shake them up.  Done!  Then I drink one in the morning, one at noon, and one around dinner time.  I do shake them again before drinking because the supplements don’t dissolve fully. They taste like sweet-salty coffee flavored milk.  It’s really good if you like sweet/salty combination foods.

So that’s my solution to the pain-in-the-ass bulk supplement situation!  I’m going to be bummed if it turns out I shouldn’t be pairing aspirin or niacinamide with coffee or milk for some reason.  I’d get over it though, so definitely tell me if that’s the case.

HCLFDE – Resumed

Ok, I took a couple days off from tracking everything, which was apparently all I needed, because now it’s fun again.  I’ve again started my High Carb Low Fat Diabetes Experiment.  I tried this before and was interrupted by a stomach bug which destabilized my system and added a confounding variable for about a week.  I stopped the experiment and now I’m ready to pick it up again.

After eating pretty much whatever I wanted for a week or so my fasting blood sugar was back up to 140 yesterday morning.  Yesterday I limited fat to 69.2g (28% of total calories) and today’s fasting blood sugar was 121.  Tomorrow I’m sure it’ll be below 120 again.  Will update with results.

On a side note: You know what’s really delicious?  1/2 cup of Nonfat Greek yogurt (I use Dannon Oikos brand because it doesn’t have a bunch of additives), 2T fructose powder (or sugar), and 1T cocoa powder.  It’s my new favorite thing.

Oh and HOLY SMOKES I feel so much better being off starches again.  It took about 3 days for my mood to completely recover back to where I’m smiling for no reason.  That stuff has a terrible effect on me.  More on that later.

High Sugar Low Fat Diabetes Experiment – Day 7 (Updated)

Well, my stomach bug/food poisoning seems to be abating, finally.  I was not in good shape the last 3 days.  I still got hungry and kept eating, but yesterday I ate only what really sounded ok – so, not much in the way of coffee, milk, and OJ, which have otherwise become my staples.  I ate a bunch of chocolate.  So my Cronometer ratios are off for yesterday – here they are:

  • Calories – 1457
  • Protein – 100.1g (28.7%)
  • Carb – 116.8g (31.4%)
  • Fat – 65g (39.9%)

So, not as low-fat as I would have liked, but I just wasn’t going to force myself to eat things that didn’t sound good when I was sick.

Today the scale was down a couple more pounds, to 203.9 lbs.  Again, may be due to dehydation, although I’ve been making a conscious effort to keep drinking water.  Fasting blood sugar this morning was 113.

So it seems I’m on to something here – my fasting blood sugar has taken a turn for the better since I started reducing fat.

Continuing on.

Update: Midnight

Well, I’ve finally recovered from my illness.  I feel great now!

Macros today:

  • Calories – 2017
  • Protein – 84.9g (17%)
  • Carb – 263.1g (52%)
  • Fat – 71g (31%)

I just let myself eat what I wanted today – including potatoes and 1/4 of a grilled cheese sandwich (Sacrebleu! Starches!).  Also didn’t want milk today at all.  I let my poor recovering stomach make the decisions today.  Tomorrow back to sweetened milk and coffee, which will tilt the ratios back in favor of carbs/proteins again.

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.

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.