Why does Danny Roddy recommend sugar to reduce stress/estrogen? page 55

[Ika]

Thank you for the link, Paleobird : ) Yes, I have watched Dr. Wahl's video; her story is definitely inspirational! I read your "Friday Success Story" here on MDA as well--you are quite an inspiration yourself! Love the panties ; )

I didn't mean to say that I think Primal always has to be low-carb--I was just saying that is how I took it when I first started learning about nutrition; it just seemed like that was kind of the general mind-set in the paleo/Primal community online at that time.

What I am interested in hearing more about is the difference between a fat-burning and sugar-burning metabolism, since I have heard very convincing arguments for both sides (especially in regards to which is better for people with MS or other chronic diseases), and both sides seem to have a decent amount of passionate supporters, for whom their respective ways of eating seem to work very well. For instance, what are the reasons people say a fat-burning metabolism are better? Can someone then explain what is wrong with these reasons, and why? And visca-versa, with a sugar burning metabolism. I want to understand the nuts and bolts of each better--why does fat burning work for some people, but not others? Why? And same for sugar-burning. I have read a lot of the literature from both sides of the story written by various experts, but I think it'd be helpful in understanding it better to discuss it more here.
Glad you're still hanging around Danny! : )

[Paleobird]

Hi Ika,
I highly recommend the book "The Art and Science of Low Carbohydrate Living" by Phinney and Volek.

Even they say that low carb is not for everybody. They estimate that 3/4 of the population does well on low carb and 1/4 on higher carb levels. There are lots of factors that make the difference but two major ones are your degree of insulin sensitivity/resistance and your degree of leptin sensitivity/resistance.

This is why young studs like Choco are perfectly fine with lots of watermelon and sweet potatoes. His metabolism functions like Grok. Those of us who have done some damage to our metabolisms, or are overweight , or are older may need to go lower carb.

I can see how one could have gotten the impression a while back from the forum pundits that Primal was all low carb all the time but that has really changed for the better.

The thing is, even with fruit and tubers added, a Primal diet is still lowER than the SAD fare.

I do not claim any expertise in MS specifically. That said, as Terry Wahls pointed out, it's all about the mitochondria. Oxidative stress is hard on them. As shown in that link Nechammer posted, there is a more efficient burn going on in terms of how much you put in/how much energy you get out plus there is a lot less oxidative stress going on with fat urning as compared to sugar burning.

[dannyroddy]

Can't they simplify my life and provide their own critiques based on their self-proclaimed knowledge about physiology?

This comment seemed to induce some kind of mania, so let me clarify:

I have been kind of enough to answer questions and not to link to Ray's (or his contemporaries) work when explaining mechanisms.

If I did that, no one here would benefit. Why? Because few want to read through Ray's essays—and I understand that.

We obviously have something with this thread, given its popularity, so why don't we continue it in a straightforward manner?

If counterpoints are brought up, please highlight them (as someone else suggested), or give me a summary.

Like I said, I'll have real internet tomorrow and will try to answer all the questions I missed.

[Stevenhamley]

Ika,

I think people have missed the mark or have oversimplified the 'sugar burner' vs 'fat burner' distinction in that it should be anaerobic vs aerobic. People with obesity/insulin resistance/type 2 diabetes tend to have a poor aerobic metabolism and more glycolytic enzymes. These people struggle to burn fat as the entire process requires the mitochondria and oxygen, but they also struggle to burn carbs completely as most of the energy from carbs also requires the mitochondria and oxygen. As a consequence they inefficiently convert glucose to lactate more often than healthy people. They are more dependent on this pathway and so are dependent on carbs.

What likely happens when people go Primal is some mitochondrial biogenesis occurs, which then improves the burning of both carbs and fats for energy, and so improves metabolic flexibility.

The Paleo Premise: Mitochondrial Dysfunction

[Paleobird]

Ika,

I think people have missed the mark or have oversimplified the 'sugar burner' vs 'fat burner' distinction in that it should be anaerobic vs aerobic. People with obesity/insulin resistance/type 2 diabetes tend to have a poor aerobic metabolism and more glycolytic enzymes. These people struggle to burn fat as the entire process requires the mitochondria and oxygen, but they also struggle to burn carbs completely as most of the energy from carbs also requires the mitochondria and oxygen. As a consequence they inefficiently convert glucose to lactate more often than healthy people. They are more dependent on this pathway and so are dependent on carbs.

What likely happens when people go Primal is some mitochondrial biogenesis occurs, which then improves the burning of both carbs and fats for energy, and so improves metabolic flexibility.

The Paleo Premise: Mitochondrial Dysfunction

That^^^ was an extremely well written article. Thank you for posting it. It comes at the evidence from the chemical standpoint (whereas the article Neckhammer quoted earlier focuses more on the mathematical) but they both end up saying the same thing, a paleo diet supports your mitochondria and lowers oxidative stress.

The quote from that article that jumped out at me was the one about all of these neurodegenerative conditions being exacerbated by inflammation. When my diabetic Dad went Primal, the inflammation in his extremities went down remarkably quickly. In just a couple of days the change was visible and within a week the inflammation was completely gone. Along with the inflammation leaving, so did his peripheral neuropathy pains.

[dannyroddy]

Hi Danny,

how low is it safe to go with for fat? I know you have provided macro percentages, but I am restricting calories at the moment in order to loose fat; I don't want to go higher than 2200 cals and to do this whilst fitting to 50/25/25 carb/protein/fat I have to drop my fat intake to 60grams per day, isn't this too low? How much fat do you eat? thanks

In general I probably consume less than 100 grams of fat a day, on average maybe around 2/3 of that.

I don't think fat is inherently harmful, but consuming gobs of it doesn't have any pro-metabolic effects.

While dieting you could measure your pulse and body temperature to get a sense of where your metabolic rate was at.

[dannyroddy]

You musta missed the previous links..... so back to you, please tell me where Lucas Tafur: Bioenergetics this is incorrect?[/url]

From reading that article, Tarfur is not concerned with the production of carbon dioxide and the release of free fatty acids damaging the mitochondria.

Or this by ambiomorph at paleohacks

"There is definitely a widespread view that gluconeogenesis necessarily raises cortisol beyond what is needed without gluconeogenesis. I think the evidence is softer than it appears.

It is undisputed that cortisol stimulates gluconeogenesis. See, e.g. The Physiology of Stress: Cortisol and the Hypothalamic-Pituitary-Adrenal Axis. This leads to the claim that continual gluconeogenesis requires continually raised levels of cortisol. That's not logically implied and I'm not sure it's true. For example, Dr. Eades says, in response to a related question:

[M]ost of the time during fasting, the hormone glucagon,which is the counter-regulatory hormone to insulin, drives gluconeogenesis, not the stress hormone cortisol.

This seems consistent with this primer on glucagon physiology, which says:

When hypoglycemia is produced in humans by injection of insulin, release of glucagon is stimulated along with that of other counterregulatory hormones when the plasma glucose decreases below 3.8 mM (~68 mg/dl) (Figure 11). Restoration of euglycemia is due to a compensatory increase in hepatic glucose production. Although secretion of catecholamines, growth hormone, and cortisol are stimulated along with that of glucagon, only the increases in plasma glucagon and catecholamines coincide with or precede the compensatory increase in the glucose production rate (66,67). That glucagon is the major acute glucose counterregulatory hormone is suggested by the fact that inhibition of the plasma glucagon responses by somatostatin markedly attenuates the compensatory increase in the glucose production rate and impairs restoration of euglycemia following insulin administration (Figure 12). Prevention of cortisol secretion (68), adrenergic blockade (66), adrenalectomy (65), or acute growth hormone deficiency (66) does not appreciably affect immediate glucose counterregulation. The effects of glucagon during restoration of euglycemia involves both glycogenolysis and gluconeogenesis, predominantly the former (69).

This does, suggest, however, that whenever blood sugar goes sufficiently low, cortisol rises. Note that this is no more likely to occur in a ketogenic state than a non-ketogenic state. In fact, most people report much more stable blood sugar levels on a ketogenic diet than otherwise. It may be relevant for fasting, though. If there is a regular stream of dietary protein available for conversion to glucose, blood sugar will probably not drop so low as to raise the cortisol alarm. This is consistent with Chris Kresser's post on [i]ntermittent fasting, cortisol and blood sugar, in which he says that some of his patients, already on a low carb, paleo diet, cannot successfully do intermittent fasting because of cortisol dysregulation. In these cases, he has them eat every 2-3 hours, and they improve. He never suggests, though, that they should abandon carbohydrate restriction.

Based on this information, I believe the notion that ketosis is stressful is simply a pervasive myth. Gluconeogenesis is mediated by glucagon, not cortisol. Cortisol will only be raised if there is hypoglycemia from fasting or from excess insulin. In fact, since the best way to control insulin is to lower carbs, ketogenic diets probably reduce the need for cortisol by providing better blood sugar control.

Why do people consider ketosis "stressful" to the body? - PaleoHacks.com

Just in case anyone missed this:

Glucagon is produced in the pancreas and stimulates the liver to release glycogen when blood sugar falls below the normal range. This is an early feature of low blood sugar, but the effects are potentiated by other glucocorticoids (cortisol).

An elevated concentration of glucagon accelerates lipolysis; the liberation and breakdown of fats. As I mentioned, the free fatty acids that get turned into ketones are protective, but the free fatty acids that don't reduce thyroid signaling, increases lactic acid (while reducing carbon dioxide), interfere with glucose metabolism (randle cycle), and breakdown into pro-inflammatory prostaglandins (increasing the production of estrogen and the conversion of tryptophan into serotonin).

How this proves your point, I have no idea.

[dannyroddy]

I have two questions for Danny Roddy:

1) You say that fish oil (even from wild caught salmon and cod liver..?) should be limited because it is also a PUFA. Does that mean you belive it's a myth that omega 3 oils are important for brain and heart health? I thought omega 3 oil was only bad if it was rancid.

The "benefits" of fish oil is most likely because they are so unstable that they interfere with the production of the pro-inflammatory prostaglandins. But that's in the short-term, over the long-term they suppress the immune system and have a variety of anti-metabolic, pro-stress effects.

2) Have I understood it correctly that you say, that people who have consumed too much PUFA's in their lifes will be negatively impacted if they start releasing fatty acids to the blood stream (same as if they eat PUFA), therefore it's best that they eat enough sugar to prevent that? But then how are they gonna get rid of the PUFA's from their body? When the cells die off and get replaced?

Correct.

The liver will get rid of PUFA similar to that of any other toxin.

Coconut oil can help "displace" unsaturated fats from the cell as well.

[Paleobird]

I have been kind of enough to answer questions.

I am done with this thread. If anyone would like to discuss any of these topic further with me feel free to PM. Having a discussion with someone who only makes unfounded assertions and can't be bothered to examine actual evidence to the contrary is futile.

And he thinks he being so "kind" to us. Gee, thanks, Danny.

[dannyroddy]

And he thinks he being so "kind" to us. Gee, thanks, Danny.

I live to give.