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FrederickSebastian

Ideas for breakfast

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Hi,

 

Recently I have tried to start CRON-dieting with great results.

 

One of my big problems, however, is that I started by eating 4 descent-sized salads a day but I HATE the idea of savory in the morning (especially salads) and would only have savory if it were eggs and bacon with toast which is obvious a thing for rare occasions and mainly a thing of the past.

I like the idea of having something sweet and have decided to drink Naked-brand green machine with a scoop of one of those green superfood and vitamin powders with like a million things in it with a teaspoon of matcha tea. Is this a good idea or is it too much sugar? I have no idea if I should be drinking the Naked-brand veggie and fruit juice or just use my juicer (which would be less practical and more expensive -- not to mention time-consuming)

 

What do you think? Any suggestions on tasty sweet or non-savory non-salad (unless it's fruit salad) items for breakfast?

 

I'd appreciate any help!

 

Thanks,

 

Fred.

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Sugars are being pretty much demonized by the recent keto craze, but the truth is that simple and complex sugars are abundant in nature and have been consumed traditionally in the blue zones and according to the scientific literature they are not directly responsible of overweight by the insulin theory of obesity (simple and attractive but apparently unconfirmed by lots of experiments) . So, unless you suffer of impaired glucose tolerance, with overly high glycemic peaks after ingestion of carbs, a little natural sugar (which in my opinion, contrary to some vegan doctors, includes honey, dark muscovado and so on) cannot be detrimental to health, on the contrary it increases palatability hence adherence to the diet. Besides, you can always add stevia and erithritol which are natural non caloric sweeteners.

Your drink sounds great, although I have no clue about its carbs content.

Fresh fruit like oranges and apples are also great for breakfast. Soy yogurt with a little honey or soy milk blended with thickeners like soaked oats, psyllium fiber and dark honey and citrus rinds is exquisite an low-caloric.

One apple with skin plus one pound unsweetened soy yogurt with a little dark honey is one example of sweet breakfast which is nourishing and relatively low carb as well.

 

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The appropriate amount of sugar varies person to person based on their current state of health and so many other factors.  But it is simple to find out what is right for you.  You can get a blood sugar testing kit as used by diabetics, often for less than $20 in the US.  Test your blood sugar, eat something, wait an hour and test it again.  My goal is to keep my blood sugar in the range the body aggressively tries to defend, which is considered the acceptable range for healthy fasting blood sugar 60-100 mg/dl.  Others are ok with postprandial blood sugar in the pre-diabetic range, up to 125 mg/dl.  Most agree that levels above 140 mg/dl are significantly harmful and should be avoided.  The foods that trigger blood sugar spikes vary from person to person.  One may be ok with breads but have trouble with sugary fruits while another is just the opposite.

I had progressed almost to the threshhold of diabetes and suffered a large number of its comorbidities.  Dropping my blood sugar back to the normal range through carbohydrate restriction fixed my health issues and has allowed me to dramatically improve my body composition and regain muscle despite having a supposedly progressive untreatable genetic neuromuscular wasting disease.  Doctors largely ignore prediabetic blood sugar because they are looking for indication that it is time to prescribe medication.  Diabetes medications are blunt tools which do not impart fine blood sugar control.  They are used to bring acutely dangerous diabetic blood sugar levels into the chronically dangerous prediabetic range.  Attempting to drive blood sugar with drugs into the healthy range risks acutely dangerous hypoglycemic episodes.  Actually hypoglycemia is only a threat to people not in ketosis and some type 1 diabetics are now leveraging that to be able to achieve normal blood sugar levels with injected insulin with significant improvement in health.

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What I do I look at the official American Diabetes Association guidelines, 2018. According to such credible publication, the prediabetes threshold is a spike of 140 to 199 mg/dL after 2 hours from the ingestion of a solution of 75 g of pure glucose. Whereas prediabetes with fasting glicemia is defined within the range 100-125 mg/dL.

Of course I never ingest pure glucose but when I measure my glycemia, I do it after 2 hours from the meal so I have a benchmark to compare my values to. I no longer measure it after 1 hour.

 

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On 4/3/2019 at 2:41 PM, mccoy said:

What I do I look at the official American Diabetes Association guidelines, 2018. According to such credible publication, the prediabetes threshold is a spike of 140 to 199 mg/dL after 2 hours from the ingestion of a solution of 75 g of pure glucose.

My goal is optimal health as opposed to pushing my luck up to the edge of a state of disease.  The ADA threshholds are defined based on cost effectiveness of diagnosis and treatment with respect to acute damage, not based on maintenance of optimal health, much like standards for toxins in food and water are set based on acute damage and economic considerations not on levels that preserve optimal health with chronic lifetime exposure.  Here's an example of evaluating HbA1c threshholds:

Alternative HbA1c Cutoffs to Identify High-Risk Adults for Diabetes Prevention A Cost-Effectiveness Perspective

Quote

Conclusions: Lowering the HbA1c cutoff for prediabetes leads to less cost-effective preventive interventions. Assuming a conventional $50,000/QALY cost-effectiveness benchmark, the HbA1c cutoffs of 5.7% and higher were found to be cost effective. Lowering the cutoff from 5.7% to 5.6% also may be cost effective, however, if the costs of preventive interventions were to be lowered.

 

Here's a position paper that explores the topic of glycemia and health with references that might make you reconsider the desirability of allowing your blood glucose to spike high for up to 2 hours after every meal.

Diagnosis and Management of Prediabetes in the Continuum of Hyperglycemia—When Do the Risks of Diabetes Begin? A Consensus Statement From the American College of Endocrinology and the American Association of Clinical Endocrinologists

Quote

Prediabetes currently refers to people who have IFG (100-125 mg/dL [5.6-6.9 mmol/L]), IGT (2-hour postglucose load, 140-199 mg/dL [7.8-11 mmol/L]), or both.
...
Presently, diabetes is diagnosed somewhat arbitrarily on the basis of the glucose level associated with the eventual appearance of characteristic end-organ complications, specifically retinopathy. Currently, diabetes may be diagnosed at a fasting plasma glucose level of 126 mg/dL (7 mmol/L) or higher or a 2-hour postglucose challenge plasma glucose concentration of 200 mg/dL (11.1 mmol/L) or higher (17,18). However, in large population studies, values for both normal fasting and 2-hour plasma glucose levels are considerably lower than these thresholds for diagnosing diabetes. The upper limit of normal fasting plasma glucose is widely believed to be 99 mg/dL (5.5 mmol/L) although metabolic and vascular abnormalities have been described recently at values less than that. Similarly, 2-hour postglucose levels less than 140 mg/dL (7.8 mmol/L) are believed to be within the reference range. Whatever label is given to the “gap” in glycemic status between normal and diabetes, the data indicate that, for many individuals, these glucose levels are not benign and may herald overt type 2 diabetes and CVD (19,20), as well as microvascular complications (2,3). Thus, the ill-defined area in fasting glucose of 100 to 125 mg/dL (5.6-6.9 mmol/L) and 2-hour levels of 140 to 199 mg/dL (7.8-11 mmol/L) is thought to describe a prediabetic range, where some degree of increased microvascular and macrovascular complications of diabetes has been described (21,22).

This intermediate state of prediabetes constitutes inherent disease risk. The progression to diabetes for patients with IGT is 6% to 10% per year, and for persons with both IFG and IGT, the cumulative incidence of diabetes by 6 years may be as high as 65% (compared with levels on the order of 5% for those with normal glucose levels at baseline) (23). Approximately half of patients with IGT meet the National Cholesterol Education Program (NCEP) criteria for the diagnosis of metabolic syndrome (24). Numerous investigations indicate that the risk of CVD maintains a linear association with glycemia well below the present diagnostic threshold for type 2 diabetes and extends to lower glucose levels than those defined by the criteria for the diagnosis of IFG and IGT (25,26) into the range of glucose otherwise considered normal (27). In addition, the CVD event rate in epidemiologic studies, such as AusDiab (Australian Diabetes, Obesity, and Lifestyle Study) (25) and Framingham (20) and intervention studies such as STOP-NIDDM (Study to Prevent Non–Insulin-Dependent Diabetes Mellitus) (14) and DREAM (Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication) (10), suggest nearly a doubling of cardiovascular risk in prediabetes compared with what would be expected for individuals without IFG or IGT.

 

Edited by Todd Allen

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Todd, I agree that the prediabetic zone is not a safe zone and the target should be to take those values down to the normality range, if we exhibit such prediabetic values.

What I do not agree upon is the absolute demonization of glucose spikes, as in many advocates of the low carb regimen, Peter Attia included.

Also, the glucose concentrations should be  compared to the insulin concentration present at the same time, as Peter Attia himself underlines ( I agree on that).

Unless unrefutable evidence is presented, I cannot be convinced that keeping glycemia and insulin as low as possible improves necessarily health and longevity. An optimum should exist, and such optimum may even vary within individuals and lifestyles.

Also, lowering at all costs glycemia makes it easy to increase cholesterolemia, if so we should decide what's worst.

Anoter issue: it's not a mistery that chronical deprivation of carbs makes people glucose-intolerant. I'm not sure that's a desirable trait.

Unfortunately, in todays' world of keto-rampage, many opinions are biased and it's not very easy to discern which studies are really credible.

 

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On 4/6/2019 at 10:16 AM, mccoy said:

What I do not agree upon is the absolute demonization of glucose spikes, as in many advocates of the low carb regimen, Peter Attia included.

https://med.stanford.edu/news/all-news/2018/07/diabetic-level-glucose-spikes-seen-in-healthy-people.html

Quote

“We saw that some folks who think they’re healthy actually are misregulating glucose — sometimes at the same severity of people with diabetes — and they have no idea,” Snyder said.

...

What’s more, nearly everyone spiked after eating the cereal.

“We saw that 80 percent of our participants spiked after eating a bowl of cornflakes and milk,” Snyder said. “Make of that what you will, but my own personal belief is it’s probably not such a great thing for everyone to be eating.”

 

High blood sugar is getting a lot of attention because it is an issue for the MAJORITY of adults, at least in the US:
diabetics    age 45-64 17.0%, 65+ 25.2%
prediabetics age 45-64 40.9%, 65+ 48.3%
TOTALS       age 45-64 57.9%, 65+ 73.5%

statistics taken from:
https://www.cdc.gov/diabetes/data/statistics-report/diagnosed-undiagnosed.html
https://www.cdc.gov/diabetes/data/statistics-report/prevalence.html

So roughly 3/4s of seniors are prediabetic and the report I posted from the endocrinologists society finds increased risk of CVD from hyperglycemia begins below the criteria for prediabetes and many with normal blood sugar have diabetic spikes after a bowl of cornflakes...

 

On 4/6/2019 at 10:16 AM, mccoy said:

Also, lowering at all costs glycemia makes it easy to increase cholesterolemia, if so we should decide what's worst.

Anoter issue: it's not a mistery that chronical deprivation of carbs makes people glucose-intolerant. I'm not sure that's a desirable trait.

Study after study finds improved cholesterol profiles of people on ketogenic diets.  HDL up strongly, triglycerides down strongly, LDL sometimes up sometimes down but consistently a better profile - larger particle size, reduced oxidation.  Markers of inflammation such as hs-CRP also consistently improve.  These factors more strongly correlate with cardiovascular risk than the calculated LDL-C of a standard lipid panel and well formulated ketogenic diets are widely recognized to potently reduce CVD risk.

As in fasting aggressive carbohydrate restriction produces a short term insulin resistance in muscle to spare glucose for the central nervous system.  This is a healthy, essential process that lowers the need for protein sourced gluconeogenesis sparing muscle tissue the largest reservoir of protein.  After a day or two of glycogen repletion this glucose sparing mechanism shuts down.

Ketogenic diets, especially when unhealthy refined vegetable oils are excluded, dramatically improve insulin sensitivity and glucose tolerance.  There are studies showing problems with "high fat diets" usually in inbred mice fed highly unnatural diets of sucrose, inflammatory casein for protein and refined soy or corn oil.  Note, HFDs are typically only 40-45% fat and still 40%+ carbs often half or more being sugar.  In such cases feeding them more starch instead of toxic vegetable oils would be healthier though I bet a more natural mouse diet of fatty grubs, nuts and seeds would produce health instead of disease.

 

Edited by Todd Allen

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Todd, there are also anecdotal but real-life reports of patients with LDL and markers of inflammation over the roof after a while of ketogenic diet. Sometimes that's settled totally eliminating saturated fats, that means incurring a very restrictive diet based on EVOO (source: various podcasts from Dr. Peter Attia). Not everyone of course, but such cases do exist.

We discussed many times about keto diet, but that's to my opinion is a tool wich is not necessarily good to everyone. To those wishing to gain and keep muscle mass, for example (except maybe your singular case, and Dom D'agostino) keto diet does exactly the opposite of what wished for: inexorable.loss of bodyweight including musculoskeletal tissue. A remedy against that may be use of testosterone, that ensures muscle preservation on a keto diet, I'm not sure that's a good bargain though, unless in slightly more than physiological doses and under medical supervision.

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The article on glucotypes from Hall et al. is very interesting, I'll take time to read it in detail. 

What Snyder suggests in the article you posted though is unrealistic: continuos glucose monitors are very costly and I don't know if they can be sold to those who are not type 1 diabetics. 

The rationale though is pretty much reasonable: most people belong to the moderate glucotype, hence they may be sensitive to some foods which cause significant glycemic spikes → be careful to such foods.

I'd be interested also, and don't know if it is present in that article, to know to what extent transient spikes are detrimental to health. Not hypotheses, rather evidences if there are. I can fully agree that spikes over 140 mg/dL after 2 hours of the meal ingestion should be avoided. What about the middle ground though ?

Diets in the blue zones all abund with cereals or carbs after all, and that's a fact.

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On 4/10/2019 at 4:57 AM, mccoy said:

Todd, there are also anecdotal but real-life reports of patients with LDL and markers of inflammation over the roof after a while of ketogenic diet. Sometimes that's settled totally eliminating saturated fats, that means incurring a very restrictive diet based on EVOO (source: various podcasts from Dr. Peter Attia). Not everyone of course, but such cases do exist.

We discussed many times about keto diet, but that's to my opinion is a tool wich is not necessarily good to everyone. To those wishing to gain and keep muscle mass, for example (except maybe your singular case, and Dom D'agostino) keto diet does exactly the opposite of what wished for: inexorable.loss of bodyweight including musculoskeletal tissue. A remedy against that may be use of testosterone, that ensures muscle preservation on a keto diet, I'm not sure that's a good bargain though, unless in slightly more than physiological doses and under medical supervision.

 

Yes, LDL going up is fairly common.  The ones where it goes up dramatically tend to be people who engage more heavily in exercise and achieve low levels of body fat.L2F-rXkqoRxyPxagQxbiG5ZTHzWtz91-HDa-s5L3oiinT4xrQ1oOP9NpWtEPa5jz9m3vW2Npq2cp2R7j68oimBi1rGrdFTlHxpH5xMbJnySURzRP78ZwVyPQkWquoJ4UvTKXFeFV

I’m trending toward that pattern though not quite there yet.  My LDL ~190, HDL & TG both ~75, but I’m still roughly 20% bodyfat.  I  expect to be a full fledged member of the group by the time I hit my goal of 12%.  Low markers of inflammation are also typical for this group.  I’m already there for ESR, hsCRP, GGT, ferritin, fibrinogen and WBCs.  Some are concerned about high LDL, but there is growing evidence of decreased severity of numerous neuromuscular diseases with high LDL and I find it curious that myalgia and/or myopathy are side effects of all drugs that lower LDL: statins, fibrates, cholestyramine and even the new pcsk9 inhibitors.

Here’s an interesting recent interview with Dr. Ron Krauss where he admits how little is known about the impacts on lipids and cardiovascular risk of high fat carbohydrate restricted diets and his interest in studying the healthfulness of this pattern of high cholesterol and low triglycerides.  And he repeatedly mentions problems of high carbohydrate diets...

Here’s a paper by Eric Verdin and John Newman of the Buck Institute on actions of ketone bodies including suppression of the NLRP3 inflammasome.
A more recent presentation on this research: John Newman - Ketone Bodies As Signaling Molecules
Another presentation of this and related research: Steve Phinney - Inflammation, Nutritional Ketosis, and Metabolic Syndrome

Here are research papers suggesting the opposite of your beliefs with respect to keto and muscle:
The Effects of Ketogenic Dieting on Body Composition, Strength, Power, and Hormonal Profiles in Resistance Training Males
CONCLUSIONS: The KD can be used in combination with resistance training to cause favorable changes in body composition, performance and hormonal profiles in resistance-trained males.
The effects of ketogenic dieting on skeletal muscle and fat mass
A presentation by one of the authors: Metabolic Health Summit: Jacob Wilson, Ph.D. | The Muscle PHD

A website for keto bodybuilders

As for testosterone mine has been climbing sharply since going keto and pulsing heavier protein intake along with intense resistance training and extreme thermal stress: most recently 1950, ref. range 250-1100.  It used to concern me as testosterone has been shown to be an essential driving factor of my disease pathology and some take testosterone blocking drugs to slow disease with the most extreme case I know of is a man who opted for sex change as this disease barely affects females.  But my IGF-1 is also up strongly which I think may be protecting me from the adverse consequences of high testosterone:

Insulinlike Growth Factor (IGF)-1 Administration Ameliorates Disease Manifestations in a Mouse Model of Spinal and Bulbar Muscular Atrophy

Quote

 

We have recently shown that in vitro insulinlike growth factor (IGF)-1 activates the phosphatidylinositol 3-kinase–Akt signaling and increases AR phosphorylation at the Akt consensus site, resulting in reduced toxicity of the mutant AR (21), and that SBMA mice genetically overexpressing a noncirculating muscle-specific isoform of IGF-1 have a less severe phenotype (22).

...

We found that administration of rhIGF-1/IGFBP3 increased activation of Akt and reduced mutant AR aggregation in skeletal muscle. Moreover, it improved motor function and pathology and prolonged the lifespan of SBMA mice.

 

I like feeling like I'm 18 again since going keto and my wife is pleased with my decision to remain male.

Edited by Todd Allen

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Heck Todd, you inundated me with references but unfortunately I'm being busy and cannot examine all things.

While most bodybuilders agree that keto diet is only good before contests, I read the Wilson and Lowery article 2017 with interest.

The comparison was isocaloric, isoproteic, and only lasted 10 weeks. After that there was a carb loading in teh KD group. The results are not impressive but at least the keto group managed not to lay behind too much in strength. The results after the carb-loading period are irrelevant to a pure KD-WD comparison. 

The KD group increased its total T, but nothing has been told about free T, which is the critical factor due to the alleged increase of SHBG during keto diet.

edit: I'm reading now that insulin remained constant, so if total T increased, also free T increased. Only, the huge increase has been measured after 11 weeks, so after one week of carb loading! My suspect is that the effect is probably not due to the KD, but to the prolonged carb loading itself.

All in all, interesting but not applicable to long term situations. KD tends to decrease hunger in most people so lowers the energy so in the long run lowers fat and muscle mass. The study was probably too short.

Congratulations to those who can adhere to the keto diet for a long period of time. To me it's very much similar to the low fat diet as fat as palatability and practicality are concerned.

Your increase of T is maybe due to the high protein intake (I wonder if you take exogenous ketones), and we can say that probably free T is increased as well if you feel strong libido. Evidently the KD is good to your specific case and I'm happy about it.

Edited by mccoy

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The results in the above article are condensed in the following plots. The undisputable conclusion I draw is that a one-week carb loading after a 10-weeks carbs deprivation yields superior results than a classic high carbs, high protein diet.

 

image.png.5768d1f8c2e8bdfe566534dfb7a6adaf.png

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21 hours ago, mccoy said:

The comparison was isocaloric, isoproteic, and only lasted 10 weeks. After that there was a carb loading in teh KD group. The results are not impressive but at least the keto group managed not to lay behind too much in strength. The results after the carb-loading period are irrelevant to a pure KD-WD comparison. 

The KD group increased its total T, but nothing has been told about free T, which is the critical factor due to the alleged increase of SHBG during keto diet.

...

Your increase of T is maybe due to the high protein intake (I wonder if you take exogenous ketones), and we can say that probably free T is increased as well if you feel strong libido.

In my case free T is up modestly as SHBG rose strongly.  But albumin is also up a lot which significantly increased bioavailable T.  My average protein intake is not particularly high due to cycling between a week of aggressive caloric restriction and fasting (averaging 30 g protein/day) followed by a month of modest caloric excess (90-100 g protein/day).  I've never taken exogenous ketones.  My ketone level is high during restriction phases and liberal use of coconut oil and sometimes MCT oil is sufficient to offset the ketone lowering effect of the added protein during my anabolic phases.

Here's another presentation that at 21:50 shows greater skeletal muscle mass after a long term ketogenic diet vs a standard high carb diet without any carb loading.


I previously posted a link to a paper by Jon Ramsey on this research.  This is on mice fed a standard research diet with the low carb and keto groups swapping lard for carbohydrates.   The keto mice getting most of their calories from lard live longer and they had much lower markers of inflammation, stayed stronger, faster, better endurance, smarter, better memory, better insulin sensitivity, and greatly reduced tumors and cancer.

Edited by Todd Allen

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Todd, the topic is interesting, but probably this is the most OT series of posts in the forum.

The subdiscussion would deserve at least 2 separate, dedicated threads,

  1. one on the The article on glucotypes from Hall et al,
  2. the other the recent article with phinney and d'agostino coauthors. This one appears pretty representative as far as relatively  short terms (10 weeks) periods go and is the only one available I think on humans and resistance training. 

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On 4/10/2019 at 4:57 AM, mccoy said:

keto diet does exactly the opposite of what wished for: inexorable.loss of bodyweight including musculoskeletal tissue

 

23 hours ago, mccoy said:

The results are not impressive but at least the keto group managed not to lay behind too much in strength. The results after the carb-loading period are irrelevant to a pure KD-WD comparison.

 

10 hours ago, mccoy said:

Todd, the topic is interesting, but probably this is the most OT series of posts in the forum.

You make a declarative unsupported statement that a keto diet causes muscle wasting.

I post a study that shows a change in resistance trained athletes of muscle thickness from 5.25 to 5.50 cm in 10 weeks on a keto diet vs 5.0 to 5.18 cm on a standard diet.  Those on the keto diet did not have wasting but rather gained 1.39 times MORE than the standard diet.  And after a week of glycogen recompensation the keto group increases another 0.2 cm for a net result that is 2.65 times better growth in muscle thickness.

And your conclusion is the results are unimpressive and we've gone OT...

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Todd, I sure agree that the study shows no muscle waste (although no increase, since 0.25 cm t= 2.5 mm = 1/10 of an inch thickness is probably within the measurement error).

I can go on but to me it seems precious time wasted (on your side as well) to write in this OT thread where we cannot even retrieve the info if needed, or redirect other discussions.

I'm goingto open another specific thread right now.

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