No Fruit in My Diet?

I remember reading my baby book and seeing a note my mother wrote to the effect “hates veggies but loves his fruit“. And who wouldn’t hate Gerber’s veggies and love their sugary fruit?

Doesn’t that retro picture just make you want to eat some vegetables?

Since there was no government required (nanny state literally) nutritional labels back then it’s hard to figure out what was in the vegetables. Maybe just mushed up vegetables and preservatives? In any event, they are a far cry from real food, but were made to remove choking hazards, right?

I am assuming things have improved in the last 50+ years. But maybe not. I might write a BLOG page on baby food in the future. But maybe I won’t. After all, my kids are almost all adults now. Maybe my future grandkids deserve for me to write a page???

My Later Life

For me, this childhood hatred of vegetables translated into a lifelong very low consumption of vegetables. If I wasn’t for French Fries it might have been years without any vegetables at all. And I rarely ate fruit either. I like peas but really nothing else. And I ate what I liked. Who doesn’t?

Low Carb Life

For my low carb life I discovered vegetables and eat almost any of them that grow above ground. And I love them. They taste sweet when your taste buds have been changed by keto.

I kid my kids when we go to the store that I need to buy some meat in case someone mistakes me for a vegetarian.

But I’ve had to avoid fruit due to the high sugar content being incompatible with the Low Carb diet. But how do I answer people who tell me I need to be eating fruit?

Just how bad is fruit?

Bad. in this case, is defined as how much sugar fruit contains. Now, fruit probably isn’t nearly as bad as refined sugar sources. After all, the sugar in fruit is combined with fiber (33 Fruits High in Fiber) which is said to be naturally protective.

However, most of the studies I could find were of fiber in grains but are typically supportive of eating more fiber like this one (Metabolic Effects of Dietary Fiber Consumption and Prevention of Diabetes . Martin O. Weickert Andreas F. H. Pfeiffer. The Journal of Nutrition, Volume 138, Issue 3, 1 March 2008, Pages 439–442).

Vegetables, of course, are also great sources of fiber so fruit isn’t needed to get the fiber (33 Vegetables High in Fiber).

Being totally random, I thought I’d compare a fruit I might eat to the vegetables that I do eat. I am comparing 100 g of Granny Smith Apples to 100 g of Broccoli and 100 g of Cauliflower.

Aren’t Computers Wonderful?

I found a neat tool to compare three foods for all of the known vitamins and macros.

The analysis is below but basically they are comparable for fiber and not for carbohydrates.

Nutrition Facts Comparison for:

#1 – Granny Smith Apples (Apples raw granny smith with skin) 100 grams (100g)

#2 – Broccoli (Broccoli raw) 100 grams (100g)

#3 – Cauliflower (Cauliflower raw) 100 grams (100g)

Food Number #1 #2 #3
Serving Size (Grams) 100g 100g 100g
Macronutrients
Calories 58 34 25
Fat (%DV) 0.19g
(0%)
0.37g
(1%)
0.28g
(0%)
Saturated Fat (%DV) ~g
(0%)
0.039g
(0%)
0.13g
(1%)
Cholesterol (%DV) ~mg
(0%)
0mg
(0%)
0mg
(0%)
Carbs (%DV) 13.6g
(5%)
6.6g
(2%)
5g
(2%)
Fiber (%DV) 2.8g
(11%)
2.6g
(10%)
2g
(8%)
Net-Carbs 10.8g 4g 3g
Sugar 9.6g 1.7g 1.9g
Protein 0.4g
(1%)
2.8g
(6%)
1.9g
(4%)
Vitamins
Vitamin A (%DV) 100IU
(2%)
623IU
(12%)
0IU
(0%)
Retinol Equiv. 5μg 31μg 0μg
Retinol ~μg 0μg 0μg
Alpha-Carotene 0μg 25μg 0μg
Beta-Carotene 59μg 361μg 0μg
Beta-cryptoxanthin 2μg 1μg 0μg
Vitamin B1 (%DV)
Thiamin
0.019mg
(1%)
0.071mg
(5%)
0.05mg
(3%)
Vitamin B2 (%DV)
Riboflavin
0.025mg
(1%)
0.117mg
(7%)
0.06mg
(4%)
Vitamin B3 (%DV)
Niacin
0.126mg
(1%)
0.639mg
(3%)
0.507mg
(3%)
Vitamin B5 (%DV)
Pantothenic Acid
0.056mg
(1%)
0.573mg
(6%)
0.667mg
(7%)
Vitamin B6 (%DV) 0.037mg
(2%)
0.175mg
(9%)
0.184mg
(9%)
Vitamin B9 (%DV)
Folate
3μg
(1%)
63μg
(16%)
57μg
(14%)
Folic Acid μg μg μg
Food Folate 3μg 63μg 57μg
Dietary Folate Equivalents ~μg 63μg 57μg
Vitamin B12 (%DV)
Cobalamin
~μg
(0%)
0μg
(0%)
0μg
(0%)
Vitamin C (%DV) ~mg
(0%)
89.2mg
(149%)
48.2mg
(80%)
Vitamin D (%DV) ~IU
~μg
(0%)
0IU
0μg
(0%)
0IU
0μg
(0%)
Vitamin D2 (%DV)
Ergocalciferol
~IU
~μg
~IU
~μg
~IU
~μg
Vitamin D3 (%DV)
Cholecalciferol
~IU
~μg
~IU
~μg
~IU
~μg
Vitamin E (%DV) 0.18mg
(1%)
0.78mg
(4%)
0.08mg
(0%)
Vitamin K (%DV) 3.2μg
(4%)
101.6μg
(127%)
15.5μg
(19%)
K1 – Dihydrophyllo-quinone 0μg 0μg 0μg
K2 – Menaquinone-4 ~μg ~μg 0μg
Choline
(% Adequate Intake)
3.4mg
(1%)
18.7mg
(3%)
44.3mg
(8%)
Lycopene 0μg 0μg 0μg
Lutein + Zeaxanthin 64μg 1403μg 1μg
Minerals
Calcium (%DV) 5mg
(1%)
47mg
(5%)
22mg
(2%)
Copper (%DV) 0.031mg
(2%)
0.049mg
(2%)
0.039mg
(2%)
Iron (%DV) 0.15mg
(1%)
0.73mg
(4%)
0.42mg
(2%)
Potassium (%DV) 120mg
(3%)
316mg
(9%)
299mg
(9%)
Phosphorus (%DV) 12mg
(1%)
66mg
(7%)
44mg
(4%)
Magnesium (%DV) 5mg
(1%)
21mg
(5%)
15mg
(4%)
Manganese (%DV) 0.044mg
(2%)
0.21mg
(11%)
0.155mg
(8%)
Sodium (%DV) 1mg
(0%)
33mg
(1%)
30mg
(1%)
Selenium (%DV) 0.1μg
(0%)
2.5μg
(4%)
0.6μg
(1%)
Zinc (%DV) 0.04mg
(0%)
0.41mg
(3%)
0.27mg
(2%)
Carbs and Sugars
Starch 0.05g 0g ~g
Sucrose 1.93g 0.1g 0g
Glucose 2.66g 0.49g 0.94g
Fructose 5g 0.68g 0.97g
Lactose 0g 0.21g 0g
Maltose 0g 0.21g 0g
Galactose 0g 0g 0g
Fatty Acids
Omega 3 to Omega 6 Ratio ~ ~ 0.94
Omega 6 to Omega 3 Ratio ~ 0 1.07
Total Omega 3s 0mg 21mg 15mg
18D3 Linolenic ~mg 21mg 15mg
18D3CN3 Alpha Linolenic(ALA) ~mg ~mg 15mg
18D4 Stearidonic (SDA) mg 0mg 0mg
20D3N3 Eicosatrienoic ~mg ~mg 0mg
20D5 Eicosapent-aenoic (EPA) ~mg 0mg 0mg
22D5 Docosapent-aenoic (DPA) ~mg 0mg 0mg
22D6 Docosahex-aenoic (DHA) ~mg 0mg 0mg
Total Omega 6s 0mg 0mg 16mg
18D2 ~mg 17mg 16mg
18D2CN6 Linoleic (LA) ~mg ~mg 13mg
18D2CLA Conjugated Linoleic (CLA) ~mg ~mg 3mg
18D3CN6 Gamma-linolenic (GLA) ~mg 0mg 0mg
20D2CN6 Eicosadienoic ~mg 0mg 0mg
20D3N6 Di-homo-gamma-linolenic (DGLA) ~mg ~mg 0mg
20D4N6 Arachidonic (AA) ~mg ~mg ~mg
22D4 Adrenic (AA) ~mg ~mg 0mg
Essential Amino Acids
Histidine
(%RDI)
~mg
(0%)
59mg
(8%)
56mg
(8%)
Isoleucine
(%RDI)
~mg
(0%)
79mg
(6%)
71mg
(5%)
Leucine
(%RDI)
~mg
(0%)
129mg
(5%)
106mg
(4%)
Lysine
(%RDI)
~mg
(0%)
135mg
(6%)
217mg
(10%)
Methionine
(%RDI)
~mg
(0%)
38mg
(5%)
20mg
(3%)
Phenylalanine
(%RDI)
~mg
(0%)
117mg
(13%)
65mg
(7%)
Threonine
(%RDI)
~mg
(0%)
88mg
(8%)
76mg
(7%)
Tryptophan
(%RDI)
~mg
(0%)
33mg
(12%)
20mg
(7%)
Valine
(%RDI)
~mg
(0%)
125mg
(7%)
125mg
(7%)
More Amino Acids
Arginine ~mg 191mg 86mg
Alanine ~mg 104mg 116mg
Aspartic Acid mg mg mg
Cystine
(%RDI)
~mg
(0%)
28mg
(10%)
20mg
(7%)
Glutamic Acid mg mg mg
Glycine ~mg 89mg 71mg
Proline ~mg 110mg 71mg
Serine mg 121mg 86mg
Tyrosine
(%RDI)
~mg
(0%)
50mg
(6%)
51mg
(6%)
Hydroxy-proline ~mg ~mg ~mg
Other
Ash 0.29g 0.87g 0.76g
Water 85.46g 89.3g 92.07g
Alcohol ~g 0g 0g
Caffeine ~mg 0mg 0mg
Theobromine ~mg 0mg 0mg
Fluoride ~μg ~μg 1μg
Stats
Percent of
Daily Calorie Target
2.9% 1.7% 1.25%
Percent Water 85.5% 89.3% 92.1%
Protein to Carb Ratio (g/g) 0.03 0.42 0.38

Studying Research – Part 3 – Study Details

We looked at the summary of a study in Part 2. In this part we will look at the details of this particular study (Annals of Internal Medicine Logo, 18 MAY 2004. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: A Randomized, Controlled Trial.
William S. Yancy Jr., MD, MHS; Maren K. Olsen, PhD; John R. Guyton, MD; Ronna P. Bakst, RD; Eric C. Westman, MD, MHS).

The reason for this particular study is further explained.

However, until recently, available data on low-carbohydrate diets came from small studies of short duration, most of which were uncontrolled.

Also our speculation of the alternate Low Fat (LF) diet was based on common recommendations at the time for a diet:

… low-fat, low-cholesterol, reduced-calorie diet commonly used to induce weight loss and decrease serum lipid levels

The participant requirements were people who were fairly messed up but had not been medicated for their health conditions. The participants were selected if they had:

  •  elevated lipid levels (total cholesterol level > 5.17 mmol/L [>200 mg/dL]
  • low-density lipoprotein [LDL] cholesterol level > 3.36 mmol/L [>130 mg/dL]
  • OR triglyceride level > 2.26 mmol/L [200 mg/dL]),

LC Group Diet

Unlike the HG group which was on a caloric restriction, the LC Group was allowed to each as much as they wanted but with certain restrictions:

Participants were permitted unlimited amounts of animal foods (meat, fowl, fish, and shellfish), unlimited eggs, 4 oz of hard cheese, 2 cups of salad vegetables (such as lettuce, spinach, or celery), and 1 cup of low-carbohydrate vegetables (such as broccoli, cauliflower, or squash) daily. Participants were encouraged to drink 6 to 8 glasses of water daily. When participants were halfway to their goal body weight (determined at the week 10 visit with assistance from research personnel), they were advised to add approximately 5 g of carbohydrates to their daily intake each week until they reached a level at which body weight was maintained.

Supplements described

To simulate the practice of the study sponsor, the low-carbohydrate diet group also received daily nutritional supplements (multivitamin, essential oils, diet formulation, and chromium picolinate…

Controlling the number of variables in an experiment is crucial. This list is problematic since it just increases the number of variables. Perhaps one of the items in that group caused the difference? Any why couldn’t most if not all of those items be given to both group?

Completion Rates

The LF group was on a calorie restricted regiment which may explain the poorer completion rate compared to the LC group. The LF…

recommended energy intake was 2.1 to 4.2 MJ (500 to 1000 kcal) less than the participant’s calculated energy intake for weight maintenance (body weight in pounds × 10)

So a typical 200 lb person was put on a 1500 calorie diet for 24 weeks and failed. Not much of a surprise to most of us. Interestingly, the LC group ended up eating less calories a day than the calorie restricted LF group:

The estimated daily energy intake was 6.14 ± 1.37 MJ (1461.0 ± 325.7 kcal) in the low-carbohydrate diet group and 6.31 ± 0.68 MJ (1502.0 ± 162.1 kcal) in the low-fat diet group.

Dietary Macros

The macros weren’t explicitly specified (just LC and LF goals) but the results were:

The low-carbohydrate diet group consumed a mean (±SD) of 29.5 ± 11.1 g of carbohydrates (8% of daily energy intake), 97.9 ± 24.3 g of protein (26% of daily energy intake), and 110.6 ± 27.3 g of fat (68% of daily energy intake) daily.

The low-fat diet group consumed 197.6 ± 34.2 g of carbohydrates (52% of daily energy intake), 70.5 ± 9.7 g of protein (19% of daily energy intake), and 48.9 ± 12.0 g of fat (29% of daily energy intake) daily.

So the LC group was eating quite a bit more protein than the LF group but the LF group was eating the sort of amount of protein that is the recommended amount.

Serum Lipid Levels

The LC results were spectacular. The only “negative” was increased LDL (Cholesterol and Low Carb Diets). In fact, the increase in LDL caused two participants to drop out over concerns about their LDL increase from their doctors. However, the number that really matters is the ratio of triglycerides to HDL which improved on both diets, but dramatically so on LC. Numbers over 3.7 are not good. Only LC reduced the number to a very good number.

Studying Research – Part 4 – Methodological Problems

LDL and BHB

Ran across an older study (The American Journal of Clinical Nutrition, Volume 83, Issue 5, 1 May 2006, Pages 1055–1061. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Carol S Johnston Sherrie L Tjonn Pamela D Swan Andrea White Heather Hutchins Barry Sears) which indicates that LDL is directly tied to BHB levels:

LDL cholesterol was directly correlated with blood β-hydroxybutyrate (r = 0.297, P = 0.025)

The study was only six weeks so it was too short a term to provide much of value in the critique of ketogenic low-carbohydrate diets. The main criticism was that people had a lack of energy on low carb during what we now know is the adaptation phase.

More details:

Compared with baseline, the 6-wk LDL concentrations increased in 5 KLC dieters (0.08, 0.13, 0.41, 0.44, and 0.52 mmol/L, respectively) and decreased in the remaining 4 KLC dieters (0.57 ± 0.18 mmol/L)

Another interesting point:

 Weight-adjusted REE increased in both diet groups over the 6-wk trial, but blood β-hydroxybutyrate concentrations were not correlated with REE (r = −0.014, P = 0.921), which indicates that the protein content of the diet, rather than the severity of the carbohydrate restriction, likely contributed to the elevations in REE.  These data support the contention that calorie-reduced diets high in protein facilitate weight loss, in part, by preserving the metabolic rate.

 

Blood Test Results (Jan 2018)

I got them back. 2015-09-04 was from before (while I was a diabetic). 2017-07-28 was my 1 year keto anniversary. The new test is about 18 months.

Test Range 2015
09-04
2017
07-28
2018
01-30
WBC 3.4-10.8 11.0 7.7 6.6
Lymphs (Abs) 0.7-3.1 3.8 3.1 2.5
Glucose, Serum 65-99 152 159 103
BUN/Creatinine 9-20 17 31 20
Protein, Tot, Ser 6.0-8.5 6.4 6.6 5.9
A/G Ratio 1.2-2.2 2 2.3 2.5
Total Cholesterol 100-199 159 Did not
check
240
Triglycerides 0-149 460 Did not
check
118
HDL Cholesterol >39 36 Did not
check
51
Trig/HDL
(Calculated)
12.78 2.31
VLDL 5-40 Invalid Did not
check
24
LDL Cholesterol 0-99 Invalid Did not
check
165
HbA1c 4.8-5.6 7.5 5.8 5.2
Vitamin D 30-100 14.9 Did not
check
Did not
check
Testosterone 264-916 Did not
check
Did not
check
520

Interpreting the Results

Looking at the results – overall very good results. Most important of all my goal of hacking my Type 2 Diabetes has been accomplished. My HbA1C number is not even in pre-diabetic range. It is right in the middle of the healthy range.

The Triglyceride number is went from a very unhealthy 460 a couple of years ago to a healthy 118 now. And I was on statins for lipid issues back then. Much healthier now and I am on no statins.

My Testosterone number would be a good number for a young man. Libido from Keto – check…

To see an increase in LDL is not an unusual situation on keto.  The very important ratio is triglycerides to HDL. My ratio went from 12.7 to 2.3 which is a very dramatic drop in risk of heart disease. See (The American Journal of Cardiology Volume 94, Issue 2, 15 July 2004, Pages 219-222. Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Viktor Hanak MD, Julian Munoz MD MSPH, Joe Teague MD, Alfred Stanley Jr. MD. Vera Bittner MD MSPHc):

A triglyceride/HDL cholesterol ratio of 3.8 divided the distribution of LDL phenotypes with 79% (95% confidence interval [CI] 74 to 83) of phenotype B greater than and 81% (95% CI 77 to 85) of phenotype A less than the ratio of 3.8. The ratio was reliable for identifying LDL phenotype B in men and women.

Studies on the Ketogenic Diet and Blood Biomarkers

There’s a lot of studies which been done on the positive benefits of the Ketogenic Diet on Blood Markers.

Cholesterol and Low Carb Diets

There’s long been a concern about cholesterol and Low Carb diets. For many people, Low Carb diets improve their LDL and HDL numbers. Nearly everyone has a significant increase in their HDL. But some people actually have an increase in their LDL on Low Carb diets (wrong direction).

HDL to Total Cholesterol Ratio

Sometimes the increase in LDL is small (but the wrong direction) and the increase in HDL is significant. This yields an improved ratio in spite of the increase in the LDL. That’s probably still a good thing relatively. From (the Mayo Clinic):

To calculate your cholesterol ratio, divide your high-density lipoprotein (HDL, or “good”) cholesterol number into your total cholesterol number. An optimal ratio is less than 3.5-to-1. A higher ratio means a higher risk of heart disease.

So if your Total Cholesterol goes up but the ration goes below 3.5 then the Mayo Clinic would call that a good thing.

LDL Big/Small Fluffy Particles

The LDL gives a single number for something that is more complicated. LDL consists of two types of particles, big fluffy ones and small sticky ones. The big fluffy ones don’t stick to the arteries. It’s the small sticky ones that stick to the arteries. For many of the people who have increases in LDL.

This is based on various studies like (JAMA. 1996;276(11):875-881. Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women. Christopher D. Gardner, PhD; Stephen P. Fortmann, MD; Ronald M. Krauss, MD):

Results.  —LDL size was smaller among CAD cases than controls (mean ±SD) (26.17±1.00nm vs 26.68±0.90nm;P<.001).The association was graded across control quintiles of LDL size. The significant case-control difference in LDL size was independent of levels of high-density lipoprotein cholesterol (HDL-C), non—HDL cholesterol (non-HDL-C), triglyceride, smoking, systolic blood pressure, and body mass index, but was not significant after adjusting for the ratio of total cholesterol (TC) to HDL-C (TC:HDL-C). Among all the physiological risk factors, LDL size was the best differentiator of CAD status in conditional logistic regression. However, when added to the physiological parameters above, the TC:HDL-C ratio was found to be a stronger independent predictor of CAD status.

Another study on the same subject (Geriatr Gerontol Int. 2018 Mar 7. Small dense low-density lipoprotein cholesterol is a promising biomarker for secondary prevention in older men with stable coronary artery disease.
Sakai K, Koba S, Nakamura Y, Yokota Y, Tsunoda F, Shoji M, Itoh Y, Hamazaki Y, Kobayashi Y.).

sdLDL-C was the most effective predictor of residual risk of future CE in stable coronary artery disease patients using statins and in high-risk coronary artery disease patients with diabetes or hypertriglyceridemia.

Another study (J Atheroscler Thromb. 2014;21(8):755-67. Elevated small dense low-density lipoprotein cholesterol as a predictor for future cardiovascular events in patients with stable coronary artery disease.
Nishikura T1, Koba S, Yokota Y, Hirano T, Tsunoda F, Shoji M, Hamazaki Y, Suzuki H, Itoh Y, Katagiri T, Kobayashi Y.).

These results confirm that sdLDL-C is a very promising biomarker to predict future cardiovascular events in the secondary prevention of stable CAD.

Testing for Particle Size

There is a test that can be done to differentiate the particle sizes. It is the NMR (Nuclear Magnetic Resonance) Test. From The NMR and Your Risk of Heart Disease.

The NMR uses advanced spectroscopy to uniquely provide rapid, simultaneous and direct measurement of LDL particle number and size of LDL particles, as well as a direct measurement of HDL and VLDL subclasses.  This detailed lipoprotein particle information allows clinicians to make more effective individualized treatment decisions as compared to standard lipid panel testing.

If you get an increase in LDL when you do Low Carb don’t just give up on Low Carb. Ask for the NMR test. Your doctor may not be familiar with this test. Mine was aware of the test but doesn’t regularly prescribe the test. There may be some cost associated depending on your coverage.