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Hi Rita, just listened to the thyroid webinar and found your presentation interesting but I have a couple of questions. Whilst I understand that hypothyroidism can lead to insulin resistance, so could well be a precursor to Type II diabetes, doesn’t insulin resistance usually lead to overall slightly raised BGs? So instigating the never ending slow rise in BGs because of slightly more insulin resistance and so more insulin is needed. If you suffer a spike in BG levels which then subsequently falls rapidly, wouldn’t this be more indicative of loss of phase 1 insulin release, rather than insulin resistance, if it falls rapidly then there isn’t much resistance? Phase 1 is released within the first few minutes of the stomach receiving something that requires insulin and that release is all over and done within the first 10 mins. So spiking at 20-30 mins is more likely to show that phase 1 hasn’t been adequate, and your phase 2 is actually picking up the tab and bringing your levels back down. Particularly when associated with low or normal fasting levels. I would have thought that low fasting, high spikes early that come down quickly, particularly when in someone of slim build, is more indicative of LADA, especially if the C-peptide is low or low normal. I would be really grateful if you could fill in the gaps for me. I am not a doctor or an endo, but have hypothyroidism, auto immune, low c-pep, low fasting (3.6-4.1 mmol/l), accompanied with high spikes, e.g. a banana = 4.1 prior to eating, 9.7 at 35 mins, 4.1 at 1 hour. p.s. exercise raises by BGs! HELP.
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Some interesting questions here. Insulin resistance (high insulin) and secondary hypothyroidism often go together, and if you can imagine that under conditions of insulin resistance there is an effort to downregulate at the cellular level, and this is what secondary hypothyroidism is, then this makes sense. T3 actually tends to be high in a lot of cases but a lot of this gets converted to reverse T3. Excess cortisol also does this and we see that a lot with insulin resistance patients.
So the two do go hand in hand, and they are both metabolic dysfunctions so this isn’t surprising. There’s a lot more we need to learn here about the interplay between them and oddly enough our understanding of primary hypothyroidism, hormonal deficiency in other words, is quite good, but we don’t know near enough about the secondary form, the loss of hormonal function, thyroid resistance if you will.
Phase 1 defects tend to occur in diabetics mostly because insulin stores become depleted due to persistently high blood sugar. If someone has normal fasting then we wouldn’t suspect this. A GTIR like Dr. Kraft used to run will reveal the insulin curve pretty well though.
The phase 1 period is very brief though and people tend to confuse this with a delayed insulin response in general which is something else. So if you peak at an hour or two hours instead of the typical 45 minutes this will cause blood sugar to rise, as it accumulates in the blood at a higher rate prior to clearing. This pattern is something we see a lot with type 2 to various degrees.
It’s more important to see how high insulin goes and typically it goes too high with most people, most non diabetics as well, and most people suffer from hyperinsulinemia these days. Some do have LADA though and don’t really go up much at all. Now this is more of a signaling issue than the virtually absent insulin secretion of a type 1 and there’s lots that goes into insulin signaling, but it does have an autoimmune component so testing PP insulin and getting tested for autoimmunity can be very helpful.