Guide On How To Optimize Glucose Oxidation

[InChristAlone]

Thanks so much for this article. It's great to see info on LDH. I haven't seen anyone talk about it. What happens when it is actually low? Mine is always below the reference range. In the last few yrs abnormally low 114! The range is 140-200. I had a practitioner tell me it's associated with hypoglycemia which I have had a terrible time with most of my life. I can eat crazy high carbs without experiencing elevated BG. Today after a snack with some grape juice I got super sleepy and felt a bit woozy before my heart rate picked up and my BG was only 87. Usually in the past I couldn't even catch it being low the adrenaline would come on so fast. Now it seems I'll get the typical hypoglycemia symptoms beforehand.

 

[yerrag]

Nice explanation of the processes involved, Hans.

It is heavy though on the bullet list of supplements, which a lot of people with good glucose megtabolism won't have to know if they're just eating with enough variety like you do. Many people think that gorging on supplements can take the place of balanced nutrition from eating out of the variety available in nature, but they're sadly mistaken.

This is nonetheless a good guide as for example it puts fructose in a better light, rather than it being villified in the mainstream, as it has its role in nutrition and in being helpful in good sugar metabolism.

From my personal experience, the role of internal bacterial infection plays a great role in inhibniting good glucose metabolism, and this point is often overlooked, and this article makes no mention of it. So, one could be doing everything the article writes about and still wonder what he's doing wrong. For one, NADH would be high and this would lower the ratio of the redox pair NAD+/NADH. But NADH is high because a higher NADH/NAD+ ratio favors the production of ROS needed to kill bacterial. So one could keep taking niacinamide for example, and still see no effect. That's only because one has to address the systemic bacterial infection to really see the NAD+/NADH ratio go to a natural equilibrium level where it is optimal for sugar metabolism.

But the medical business establishment don't have the tools nor the desire to make tools or tests available to identify these "hidden" bacterial infections that reside internally, if not externally. By internal I mean the blood vessels, and externally, I mean the gut. So, this hampers the effort of people to optimaize sugar metabolism and to lose weight.

 

[gaze]

Thanks so much for this article. It's great to see info on LDH. I haven't seen anyone talk about it. What happens when it is actually low? Mine is always below the reference range. In the last few yrs abnormally low 114! The range is 140-200. I had a practitioner tell me it's associated with hypoglycemia which I have had a terrible time with most of my life. I can eat crazy high carbs without experiencing elevated BG. Today after a snack with some grape juice I got super sleepy and felt a bit woozy before my heart rate picked up and my BG was only 87. Usually in the past I couldn't even catch it being low the adrenaline would come on so fast. Now it seems I'll get the typical hypoglycemia symptoms beforehand.

you high dose vit C right? look into that relationship with LDH. pretty sure it's known high dose vit C artificially lowers LDH on blood labs

 

[InChristAlone]

you high dose vit C right? look into that relationship with LDH. pretty sure it's known high dose vit C artificially lowers LDH on blood labs

Yes I forgot about that, but it should be out of my system by the morning. I also just saw that the reference range can be 104-250 so maybe my level isn't abnormally low.

 

[gaze]

Yes I forgot about that, but it should be out of my system by the morning. I also just saw that the reference range can be 104-250 so maybe my level isn't abnormally low.

i don't think it being below the range low is a problem either, in fact it may be protective, although i'm not sure if it works by lowering lactate production or if it's reacting with the LDH itself. Maybe @Amazoniac knows. but i think it's well known vit C users have low LDH:

Lactate Dehydrogenase (Blood) - Health Encyclopedia - University of Rochester Medical Center

www.urmc.rochester.edu

"Anesthetics, aspirin, narcotics, and certain other medicines can raise your LDH. Medicines with ascorbic acid (vitamin C) can decrease your LDH levels. Alcohol also can affect your LDH levels."

i don't think one night would be enough for it to normalize. maybe try not taking it for a week before your next test just to see what would happen?

 

[InChristAlone]

i don't think it being below the range low is a problem either, in fact it may be protective, although i'm not sure if it works by lowering lactose or if it's reacting with the LDH itself. but i think it's well known vit C users have low LDH:

Lactate Dehydrogenase (Blood) - Health Encyclopedia - University of Rochester Medical Center

www.urmc.rochester.edu

"Anesthetics, aspirin, narcotics, and certain other medicines can raise your LDH. Medicines with ascorbic acid (vitamin C) can decrease your LDH levels. Alcohol also can affect your LDH levels."

i don't think one night would be enough for it to normalize. maybe try not taking it for a week before your next test just to see what would happen?

Thanks, yeah I'd much rather it be just a bit low than it be too high! which is a marker for tissue damage. I will try going off it for a week or two before my next test which is actually coming up. I do yearly blood tests.

 

[Hans]

Thanks so much for this article. It's great to see info on LDH. I haven't seen anyone talk about it. What happens when it is actually low? Mine is always below the reference range. In the last few yrs abnormally low 114! The range is 140-200. I had a practitioner tell me it's associated with hypoglycemia which I have had a terrible time with most of my life. I can eat crazy high carbs without experiencing elevated BG. Today after a snack with some grape juice I got super sleepy and felt a bit woozy before my heart rate picked up and my BG was only 87. Usually in the past I couldn't even catch it being low the adrenaline would come on so fast. Now it seems I'll get the typical hypoglycemia symptoms beforehand.

Do you get hypoglycemia after any carb meal or any after certain ones? Also, what do you pair it with the might make it contribute?

 

[Hans]

Nice explanation of the processes involved, Hans.

It is heavy though on the bullet list of supplements, which a lot of people with good glucose megtabolism won't have to know if they're just eating with enough variety like you do. Many people think that gorging on supplements can take the place of balanced nutrition from eating out of the variety available in nature, but they're sadly mistaken.

This is nonetheless a good guide as for example it puts fructose in a better light, rather than it being villified in the mainstream, as it has its role in nutrition and in being helpful in good sugar metabolism.

From my personal experience, the role of internal bacterial infection plays a great role in inhibniting good glucose metabolism, and this point is often overlooked, and this article makes no mention of it. So, one could be doing everything the article writes about and still wonder what he's doing wrong. For one, NADH would be high and this would lower the ratio of the redox pair NAD+/NADH. But NADH is high because a higher NADH/NAD+ ratio favors the production of ROS needed to kill bacterial. So one could keep taking niacinamide for example, and still see no effect. That's only because one has to address the systemic bacterial infection to really see the NAD+/NADH ratio go to a natural equilibrium level where it is optimal for sugar metabolism.

But the medical business establishment don't have the tools nor the desire to make tools or tests available to identify these "hidden" bacterial infections that reside internally, if not externally. By internal I mean the blood vessels, and externally, I mean the gut. So, this hampers the effort of people to optimaize sugar metabolism and to lose weight.

Just found this study the other day, which looked at the microbiome and NAD (R), but sadly can't get the full paper.

 

[aliml]

MCD is involved in regulating malonyl-CoA levels, inhibition of MCD can limit rates of fatty acid oxidation, leading to a secondary increase in glucose oxidation

Malonyl-CoA decarboxylase - Wikipedia

en.wikipedia.org

Bouzakri et al. studied the effects of inhibiting MCD (Malonyl-CoA Decarboxylase) activity in isolated human skeletal myocytes via transfection of the cultured cells with small interfering RNAs specific to the MCD transcript (3). They show that 75% inhibition of MCD expression with this method results in a doubling of malonyl CoA levels and a clear shift from fatty acid to glucose oxidation, in effect mimicking the fasted-to-fed transition. MCD inhibition also led to reduced palmitate uptake and decreased expression of fatty acid transport protein 1; conversely, glucose uptake in both the basal and insulin-stimulated states was enhanced in association with increased cell surface levels of GLUT4. Interestingly, although insulin-stimulated glucose uptake was increased in cells with suppressed MCD expression, no enhancement in insulin signaling was detected when measured at the levels of insulin receptor substrate-1 tyrosine phosphorylation, phosphatidylinoitol 3-kinase activity, or serine phosphorylation of Akt and glycogen synthase kinase-3. These results suggest that MCD suppression encourages glucose uptake and utilization through mechanisms that are independent of the known insulin signaling pathway. Based on these findings, the authors reasonably suggest that MCD may be a therapeutic target for patients with insulin resistance and type 2 diabetes.

Other recent studies provide direct insights into the potential and also the considerable complexities of developing MCD inhibitors for diabetes therapies. Thus, in one recent study, whole animal knockout of MCD conferred resistance to diet-induced impairment of insulin action, as shown by glucose tolerance testing (6). On the other hand, an earlier report found that overexpression rather than suppression of MCD in liver of rats fed on a high-fat diet ameliorated whole-animal, liver, and muscle insulin resistance (7). A unifying explanation for these seemingly discordant findings has recently been advanced (8). In this model, ingestion of diets high in fat and carbohydrate lead to accumulation of malonyl CoA in liver, resulting in hepatic steatosis and conversion of excess fats into species associated with hepatic insulin resistance such as diacylglycerol and ceramides. Consistent with this model, overexpression of MCD in liver of high-fat–fed rats resolves hepatic steatosis and lowers circulating fatty acid levels while reversing insulin resistance (7).

In contrast, high-fat feeding actually increases rather than decreases β-oxidation in muscle due to transcriptional activation of the pathway and increased substrate supply (9). In sedentary animals, this induction appears to occur without a coordinated increase in tricarboxylic acid cycle flux, resulting in incomplete β-oxidation and accumulation of incompletely oxidized lipid intermediates that are thought to reflect mitochondrial stress (6,9). Knockout of MCD prevented incomplete fat oxidation in muscle and protected against diet-induced insulin resistance, suggesting a potential connection between mitochondrial overload and glucose intolerance (6). Surprisingly, lipid metabolism in the liver appeared to be relatively unaffected by this manipulation. Because MCD is present in three subcellular compartments, the tissue-specific consequences of its absence might reflect distinct distributions of the enzyme activity (5). In light of this possibility, it is important to emphasize that An et al. (7) overexpressed a form of the MCD gene that lacks the mitochondrial and peroxisomal targeting sequences, which, by design, resulted in liver-specific elevation of cytosolic activity. It is also noteworthy that the liver isoform of CPT-1 is 100-fold less sensitive to malonyl CoA than its counterpart in the muscle (1); this too could contribute to tissue-specific metabolic effects of MCD inhibition.

Fatty Acid Oxidation and Insulin Action: When Less Is More

Type 2 diabetes is a disease of metabolic dysregulation involving impaired uptake and utilization of glucose, altered lipid metabolism, accumulation of various

diabetes.diabetesjournals.org

 

[Motorneuron]

@Hans
In ALS, glucose metabolism is impaired ... is there more that can be done besides these tips? I had a very strong but short-lived response from lithium, it certainly inhibited that enzyme even momentarily raising the insulin (in fact I had full muscles never seen During the illness, unfortunately it only lasted a few days then it stopped working) but if the problem in the SLA were upstream in the hypofunctioning PL3K AKT path ... how could one intervene?

 

[HealingTheBody]

@Roni123@ Nice thread

 

[Roni123@]

@Roni123@ Nice thread

I read this article, later I will reread it how is your progress? I was doing great, but unfortunately Ray is right, grains have a great ability to reduce the thyroid, I was predominant on corn and wheat for carbohydrates and after a while my health went downhill. simply by eliminating the two I recovered very quickly.