Ray Peat Email Advice Depository

[Bumberleybee]

Dear Ray,

What is the best topical form of tetracycline for acne please that I can obtain in the UK from a GP?

I think the easiest thing would be an over-the-counter neomycin lotion.

 

[Bumberleybee]

Dear Ray,

If one lung is damaged by pneumonia and left with scarring and the pneumonia returns periodically, is there a protocol that may assist with prevention please? .

The liver, intestine, and lungs interact very closely, and supporting the liver with nourishment and adequate thyroid, while avoiding irritating foods such as salads, beans, and allergens, will usually prevent recurring respiratory problems.

 

[Bumberleybee]

Are there any methods of contraception that are chemical free or safe enough to use? I am thinking of using a body temp monitor in combination with condoms on fertile days, but notice condoms have a lot of unrecognisable ingredients in them which look dangerous?

Some condoms are coated with silicone lubricant, and could cause allergic or immune problems. A fitted cervical cap, as described by Barbara Seaman, is probably the ideal. Some women have had success with a plastic diaphragm coated with progesterone.

 

[Bumberleybee]

Dear Ray,

My dentist asked if I have a high sugar diet due to excess tartar since adopting a higher fruit and sugar diet.

Is there a way to help reduce this and any damage from coffee with sugar and fruit?

Rinsing the mouth right after eating.

 

[Bumberleybee]

Dear Ray,

I am struggling to control my blood sugar levels (bsl's) when eating fruits with type one diabetes.

I have read your diabetes articles.

A typical meal for me would be protein plus fruit and fats, maybe eggs with OJ and gelatine and a coffee with milk and sugar.

I get a high bsl soon after followed by a crash. I take Novorapid insulin and inject ahead of time as from trials it takes about 20 mins to move my blood sugars.

Added fat seems to slow sugar entry and I may get a low level after food followed by having to rescue levels with coca cola (UK so sugar not HFCS), then a high bsl later when everything is digested from the meal.

Is it just a case of tweaking ratios of macros to suit the injectable insulin I take?

Cynoplus has not made much difference to bsl's, pulse and temp up though.

Could you give me examples of the blood sugar changes, and how long they last, influence of time of day?

Morning 6am:

Take 10units Detemir long acting insulin
Take 1 unit Novorapid to prevent dawn phenomenon blood sugar rise

8am
Take 4 units Novorapid
Eat 400ml OJ plus gelatine
Eat 2 eggs boiled
1 mug coffee with milk and 2 heaped sugars
Bsl goes from 5mmol up to 12mmol within 20-30mins then if I leave it (no insulin correction) will drop after about an hour and a half to 3.2mmol then I need sugar.

Mid morning: large bunch grapes (about 500g) and cheese (40g) take 4 units Novorapid. Bsl spikes to around 13.5mmol then drops low 3.6mmol after a couple of hours.

Evening meal (I eat more snacks in between)
Cod and well boiled potatoes with salt and butter and runner beans and glass of OJ.

Inject 4 units Novorapid. Bsl drops within 45 mins to 3.5mmol and I drink coke to bring up. During night, bsl spikes as high as 16mmol when presumably potato has been digested or rebound reaction.

I take Detemir before bed also, 10 units (long acting insulin)

I take cynoplus through the day, 1 tablet split into 5/6 pieces plus progest exon second half of cycle and the other supplements I mentioned.

Do you have liver or brewers' yeast occasionally? Have you tried supplementing vitamin B1 and pantothenic acid? Do you use any aspirin?

I don't eat liver as it makes me very nauseas but I could try brewers yeast if it is useful for something?

I haven't tried B1 or pantothetic acid. Would this be in addition to brewers yeast?

I don't currently use aspirin but am trying to source a pure form in the UK.

Would you be able to provide approximate doses for all of the above please and let me know what they assist with?

Vitamin B1 helps to oxidize glucose, so if you try 50 or 100 mg with a meal you should watch for possible hypoglycemia from the insulin. Pantothenic acid is safe in doses of 100 or 200 mg, and helps to limit hypoglycemia. Brewers' yeast has other nutrients that help with repairing the pancreas, but can cause gas, so it's best to start by pouring hot water over an ounce or two of it, and using just the liquid.

 

[Bumberleybee]

Dear Ray,

I recently had TPO antibodies show up on a blood test. I have had type one diabetes for 28yrs.

I gave up gluten soon after the results, last August.

Just starting to eat more fructose, no grains, dairy out for now as it causes acne probably due to leaky gut from gluten. I will reintroduce later.

Is Cynomel okay to take with diabetes and TPO antibodies. I understand T4 conversion can be problematic?

I was also wondering if paying for a full thyroid blood panel would be wise to see if the antibodies have halted since avoiding gluten or would this be a waste of money?

Was your TSH tested? Usually the antibodies just mean that the thyroid gland is inflamed, and increased TSH can be responsible for that. T4 can suppress TSH protectively, but since intracellular glucose is needed for making T3, diabetes can interfere with that. I think some T3 is always appropriate with diabetes.

Thank you Ray.

Yes, TSH was 3.9, it has gone up recently. That was Aug 2015, the one prior in Sept 2014 was 0.93.

Would a full thyroid panel be worth the money? I was considering dosing T3 on symptoms alone.

I think the high TSH explains the antibodies, and a combination of T4 and T3 is usually all that’s needed; it usually takes a few months after suppressing TSH for the antibodies to decrease. Cortisol would be important to know, also estrogen and prolactin would be more informative than the common thyroid tests.

 

[Bumberleybee]

Dear Ray,

I am in the UK and wanted to obtain some T3 and T4 to start taking for type one diabetes.

The Mexican Pharmacy are only selling a product called Triyotex now.

I can't seem to find out if this is T3 or T4 or a combination.

Would this be suitable and how would I split the tablets to begin. With Cynoplus you said 5/6 pieces built up over a few weeks plus some T4 to suppress TSH.

I think Triyotex is T3, 75 mcg, which would be three times as much as Cynomel, but I haven’t tried it, and don’t know how effective it is. Usually, a 5 mcg dose of T3 with each meal is effective. Anti-aging Systems in England has a large variety of thyroid products.

 

[Bumberleybee]

Dear Ray,

I am trying to decide the best route to obtain thyroid meds for type 1 diabetes. I have cold hands and feet, pulse rate averages around 65bpm and I showed TPO antibodies, which you said is probably due to a high TSH of 3.9.

I would prefer to get a prescription but it seems my endocrinologist won't entertain that I need them based on symptoms alone.

Which product is a good one please? Cynoplus and Cytomel are no longer available from the Mexican pharmacy. I see anti ageing systems has several, just not sure which brand to order?

Brands that I have used are Armour, Cynoplus, Novotiral, and Proloid-S. People have told me they have good results from WP-thyroid and Thyroid-S. Have you tried farmaciadelnino.com?

 

[Bumberleybee]

Dear Ray,

I've just been reading your article on diabetes and wondered if you know of any cases of long standing type 1 diabetes being eradicated?

I have am just starting to read your articles, after 28yrs with T1D and adopt the anti ageing eating dirt you describe to test it.

I find fruit easy on blood sugars, quickly in and out of the blood. Starches are too unpredictable. I am of course trying to match foods to the action of an unnatural injected insulin.

Any pointers for research / reading would be greatly appreciated.

Starches and polyunsaturated fats keep stressing beta cells as they regenerate. Endotoxin and nitric oxide cause insulin resistance, besides being toxic to the beta cells, so it’s essential to keep the small intestine relatively free of bacteria. A daily raw carrot salad is helpful; well cooked mushrooms every day can help in a veriety of ways.

 

[Bumberleybee]

On type one diabetes ...

I think it’s valuable to have a blood test for vitamin D to regulate the dose; TSH can be useful, too, but it’s very important to check your temperature and pulse rate regularly to judge the effects of a thyroid supplement, since the need for it varies with season and type of activity. Has your cortisol been checked occasionally? I think it’s common for kids to be diagnosed as diabetic when they have high blood sugar following a sickness such as flu; insulin treatment can institutionalize an over-production of the stress hormones. Inflammation of the intestine (which can start with an infection) can be sustained by undigested starches, and the resulting endotoxin/nitric oxide/serotonin can cause insulin resistance, so it’s important to keep the small intestine relatively germ-free. Melons and potatoes can feed bacteria if they are present. Adequate calcium is extremely important, because of the interactions of parathyroid hormone and serotonin with stress and glucose metabolism.
Daily protein should be at least 80 grams, and fruit should provide a large part of the calories. A little vitamin B6 (10 mg) can help with amino acid metabolism.

 

[Bumberleybee]

Effects of dietary calcium on blood pressure, vascular reactivity and vascular
smooth muscle calcium efflux rate in Zucker rats.
Ambrozy SL(1), Shehin SE, Chiou CY, Sowers JR, Zemel MB.
(1)Division of Endocrinology and Hypertension, Wayne State University, Detroit,
Michigan.
Previous data from this laboratory indicate that hypertension in insulin
resistant Zucker obese rats is accompanied by an impairment in vascular smooth
muscle Ca2+ efflux. Since insulin resistant states are also generally
salt-sensitive and dietary Ca2+ reduces blood pressure in some salt-sensitive
states, we evaluated the effects of dietary Ca2+ on blood pressure and vascular
reactivity and examined whether these effects are due to increased vascular
smooth muscle Ca2+ efflux. We assigned 16 obese and 16 lean rats to a normal
(0.5%) or high (1.5%) Ca2+ diet for 28 days, following which intraarterial blood
pressure and in vitro vascular smooth muscle 45Ca efflux and vascular reactivity
responses to phenylephrine and serotonin were measured. Blood pressure was
elevated in the obese rats on both diets (P less than 0.2), and the high calcium
diet lowered both systolic and diastolic pressure in both the lean and obese rats
(P less than 0.5). Vascular reactivity was higher in the obese rats (P less than
0.2), but dietary Ca2+ exerted opposite effects on vascular reactivity to the
agonists. High Ca2+ reduced sensitivity to serotonin in the obese rats by 54% (P
less than .05) without affecting sensitivity in the lean rats. In contrast, the
high Ca2+ diet increased sensitivity to phenylephrine by 31% in both groups (P
less than .01). 45Ca efflux was lower in the obese rats compared to the lean rats
(P less than .05), and the high Ca2+ diet increased this rate by 23% in the lean,
but not the obese, rats (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Am J Physiol. 1989 Feb;256(2 Pt 2):R435-42.
Peripheral and central consequences of immobilization stress in genetically obese
Zucker rats.
Chaouloff F(1), Laude D, Merino D, Serrurier B, Elghozi JL.
(1)Laboratoire de Pharmacologie, Institut National de la Santé et de la Recherche
Médicale U7, Centre Hospitalier Universitaire, Paris, France.
Peripheral and central effects of acute and chronic immobilization stress were
measured in lean and obese Zucker female rats. Thus hypothalamic serotonergic
metabolism was analyzed by measuring the concentrations of serotonin
(5-hydroxytryptamine, 5-HT), tryptophan (TRP; the precursor of 5-HT), and
5-hydroxyindoleacetic acid (5-HIAA; 5-HT metabolite). In addition, plasma total
TRP, free fatty acid (FFA), insulin, and corticosterone concentrations were
measured. Analysis of stress-induced changes in food consumption were also
included. A single 2-h restraint stress was found to increase TRP availability in
the hypothalamus of both rats; this promoted an increase in 5-HIAA in the lean
rats and increases in 5-HT and 5-HIAA in the obese (fa/fa) rats. These
modifications were associated with marked decreases in plasma total TRP and
insulinemia in the lean and obese rats. Whereas stress triggered similar
hypercorticosteronemia and hyperglycemia, FFA was increased in the lean rats
only. Consecutive hypophagia was noted in all the rats. Twenty-four hours after
the last of the four 2-h stress sessions, hypothalamic 5-HIAA was increased in
the obese rats and plasma TRP and FFA levels decreased in both rats. Although
both groups of rats were normoglycemic, stress-induced hyperinsulinemia was
evidenced in the lean rats, thus suggesting that chronic stress promotes insulin
resistance. These metabolic variations were associated with normal food
consumption and increased body weight gains in the lean and obese Zucker rats.

Eur J Clin Pharmacol. 1979 Jul;15(6):395-9.
Improved oral glucose tolerance following antiserotonin treatment in patients
with chemical diabetes.
Ferrari C, Barbieri C, Caldara R, Magnoni V, Testori GP, Romussi M.
The effects of short-term treatment with either placebo or two serotonin
antagonists, cyproheptadine and metergoline, on oral glucose tolerance and
insulin secretion have been evaluated in normal subjects and in patients with
chemical diabetes. Placebo treatment was not associated with any significant
change in the parameters examined. Glucose tolerance in chemical diabetics was
significantly improved both after cyproheptadine and metergoline; fasting plasma
glucose was also reduced by metergoline. Treatment with the latter drug was also
associated with a significant decrease in incremental glucose area in healthy
subjects, which was not affected by cyproheptadine. Basal and glucose-stimulated
insulin secretion were not affected by either drug in any subjects.
Cyproheptadine and metergoline improve glucose metabolism in chemical diabetes
probably by reducing insulin resistance. This may depend either on decreased
secretion of counter-regulatory hormones or on a direct pharmacological action of
the drugs on glucose utilization, possibly mediated by their common
antiserotoninergic properties.

Neuroendocrinology. 1998 Jul;68(1):1-10.
Bromocriptine reduces obesity, glucose intolerance and extracellular monoamine
metabolite levels in the ventromedial hypothalamus of Syrian hamsters.
Luo S(1), Meier AH, Cincotta AH.
(1)Ergo Science Corporation, Charlestown, Mass 02129, USA. [email protected]
We examined whether reductions in body fat stores and insulin resistance in
Syrian hamsters induced by bromocriptine are associated with reductions in daily
norepinephrine (NE) and serotonin activities as indicated by their extracellular
metabolite levels in the ventromedial hypothalamus (VMH). High levels of these
monoamines within the VMH have been suspected to induce obesity and insulin
resistance. Microdialysate samples from the VMH of freely moving obese male
hamsters (BW: 208 +/- 5 g) were collected hourly over a 25-hour period before
bromocriptine treatment, during the first day of and after 2 weeks of
bromocriptine treatment (800 microg/animal daily, i.p.), and body composition and
glucose tolerance analyses were conducted before and after 2 weeks of treatments.
The microdialysate samples were analyzed by HPLC for metabolites of serotonin:
5-hydroxy-indoleacetic acid (5-HIAA), NE: 3-methoxy-4-hydroxy-phenylglycol
(MHPG), and dopamine: homovanillic acid (HVA). Bromocriptine treatment for 14
days significantly reduced body fat by 60% and areas under the glucose and
insulin curves during a glucose tolerance test by 50 and 46%, respectively.
Concurrently, extracellular VMH contents of 5-HIAA, MHPG, and HVA were reduced by
50, 29 and 66%, respectively (p < 0.05). Similarly, VMH 5-HIAA and MHPG contents
were 48 and 44% less, respectively (p < 0.05), in naturally glucose-tolerant
hamsters compared with naturally glucose-intolerant hamsters. Bromocriptine
induced reductions of body fat, and improvements in glucose intolerance may
result in part from its ability to decrease serotonin and NE activities in the
VMH.

Life Sci. 1993;53(20):1545-55.
Serotonin-mediated acute insulin resistance in the perfused rat hindlimb but not
in incubated muscle: a role for the vascular system.
Rattigan S(1), Dora KA, Colquhoun EQ, Clark MG.
(1)Department of Biochemistry, University of Tasmania, Hobart, Australia.
We have recently shown that the vasoconstrictor serotonin (5-HT) inhibits oxygen
uptake in perfused hindlimb possibly due to vascular shunting. Thus in the
present study the effect of 5-HT on insulin-mediated glucose uptake was assessed.
Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM
glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10
microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited
insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin
and 34.4% when added before insulin. In addition, 5-HT inhibited insulin-mediated
2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80%
(extensor digitorum longus). The effects of 5-HT on insulin-mediated glucose
uptake were partially reversed by vasodilation with carbachol. In contrast to the
results for the hindlimb, 10 microM 5-HT had no significant effect on either
basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM
insulin by isolated incubated soleus or extensor digitorum longus muscles. It is
concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat
hindlimb that may derive from vascular shunting not apparent when muscles are
incubated with 5-HT in vitro. These findings may have implications for the link
between hypertension and diabetes.

Proc Soc Exp Biol Med. 1991 May;197(1):44-8.
Potentiation of antigen-induced mast cell activation by 1-34 bovine parathyroid
hormone.
Simpson KM(1), Dileepan KN, Stechschulte DJ.
(1)Department of Internal Medicine, University of Kansas Medical Center, Kansas
City 66103.
Peptides such as parathyroid hormone (PTH), somatostatin, and gastrin have been
reported to stimulate mast cell mediator release. Preincubation of rat serosal
mast cells with synthetic 1-34 bovine parathyroid hormone (1-34bPTH)
significantly enhanced antigen-induced 5-hydroxytryptamine (5-HT) release.
Enhancement of 5-HT release by 1-34bPTH was dose dependent between 5 and 2000 nM.
In the absence of antigen, mean net 5-HT release was less than 1% when naive or
passively sensitized mast cells were incubated with 1000 nM 1-34bPTH for time
intervals up to 90 min. These findings indicate that 1-34bPTH, at relatively low
concentration, potentiates antigen-induced 5-HT release from mast cells.

Domest Anim Endocrinol. 2013 May;44(4):176-84.
Feeding 5-hydroxy-l-tryptophan during the transition from pregnancy to lactation
increases calcium mobilization from bone in rats.
Laporta J(1), Peters TL, Weaver SR, Merriman KE, Hernandez LL.
(1)Department of Dairy Science, University of Wisconsin-Madison, Madison, WI
53706, USA.
An increasing demand for calcium during pregnancy and lactation can result in
both clinical and subclinical hypocalcemia during the early lactation period in
several mammalian species, in particular the dairy cow. Serotonin (5-HT) was
recently identified as a regulator of lactation and bone turnover. The purpose of
this study was to determine whether supplementation of the maternal diet with a
5-HT precursor would increase maternal bone turnover and calcium mobilization to
maintain appropriate circulating maternal concentrations of ionized calcium
during lactation. Female Sprague-Dawley rats (n = 30) were fed either a control
diet (n = 15) or a diet supplemented with the 5-HT precursor 5-hydroxytryptophan
(5-HTP, 0.2%; n = 15) from day 13 of pregnancy through day 9 of lactation.
Maternal serum and plasma (day 1 and day 9 of lactation), milk and pup weight
(daily), mammary gland and bone tissue (day 9 of lactation) were collected for
analysis. The 5-HTP diet elevated circulating maternal concentrations of 5-HT on
day 1 and day 9 of lactation and parathyroid hormone related-protein (PTHrP) on
day 9 of lactation (P < 0.033). In addition, 5-HTP supplementation increased
total serum calcium concentrations on day 1 of lactation and total milk calcium
concentration on day 9 of lactation (P < 0.032). Supplemental 5-HTP did not alter
milk yield, maternal body weight, mammary gland structure, or pup litter weights
(P > 0.05). Supplemental 5-HTP also resulted in increased concentrations of
mammary 5-HT and PTHrP, as well as increased mRNA expression of rate-limiting
enzyme in 5-HT synthesis, tryptophan hydroxylase 1, and Pthrp mRNA on day 9 of
lactation (P < 0.028). In addition, supplementation of 5-HTP resulted in
increased mRNA expression of maternal mammary calcium transporters and resorption
of bone in the femur, indicated by increase osteoclast number and diameter
as well as mRNA expression of classical markers of bone resorption on day 9 of
lactation (P < 0.048). These results show that increasing 5-HT biosynthesis
during the transition from pregnancy to lactation could be a potential
therapeutic target to explore for prevention of subclinical and clinical
hypocalcemia.
Copyright © 2013 Elsevier Inc. All rights reserved.

Trends Endocrinol Metab. 2014 Jan;25(1):34-41.
New concepts of breast cell communication to bone.
Horseman ND(1), Hernandez LL(2).
(1)Department of Molecular and Cellular Physiology, Program in Systems Biology
and Physiology, University of Cincinnati, Cincinnati, OH 45267-0576, USA.
Electronic address: [email protected]. (2)Department of Dairy Science,
University of Wisconsin, Madison, Madison, WI 53706-1205, USA.
Lactation is the most extreme case of normal physiological bone loss during a
lifetime, and breast cancers have a strong tendency to metastasize to bone. In
both the physiological and pathological circumstances, parathyroid
hormone-related peptide (PTHrP) plays a central role. Until recently there were
no regulatory mechanisms to explain the induction of endocrine PTHrP secretion
from breast cells during lactation. The mammary epithelium possesses a local
serotonin signaling system which drives PTHrP expression during lactation and in
breast cancer cells. The mammary gland serotonin system is highly induced in
response to alveolar dilation due to milk secretion. Discovery of serotonergic
control of PTHrP suggests that it may be possible to manipulate the
breast-to-bone axis by targeting serotonin signaling.
Copyright © 2013 Elsevier Ltd. All rights reserved.

Iran J Kidney Dis. 2013 Jan;7(1):36-41.
Plasma serotonin and markers of bone formation and bone resorption in
hemodialysis patients.
Eleftheriadis T(1), Antoniadi G, Liakopoulos V, Sparopoulou T, Stefanidis I,
Galaktidou G.
(1)Department of Nephrology, Medical School, University of Thessaly, Larissa,
Greece. [email protected]
INTRODUCTION: Serotonin receptors are present in osteoblasts and osteoclasts, and
serotonin affects bone metabolism. The association of plasma serotonin with
markers of bone formation and bone resorption in hemodialysis patients was
evaluated.
MATERIALS AND METHODS: Twenty-four hemodialysis patients (11 diabetics) and 22
healthy volunteers were enrolled into the study. Serotonin was assessed in
platelet-free plasma, whereas the markers of osteoblastic activity N-terminal
midfragment osteocalcin and total procollagen type-1 aminoterminal propeptide as
well as the marker of osteoclastic activity beta-isomerized C-terminal
cross-linked peptide of collagen type I were measured in serum. Serum intact
parathyroid hormone was also assessed.
RESULTS: Serotonin did not significantly differ between hemodialysis patients and
healthy volunteers. All evaluated markers of bone metabolism and intact
parathyroid hormone were much higher in hemodialysis patients. Serotonin was
significantly correlated with all evaluated markers of bone metabolism in
hemodialysis patients. Serotonin was reversely related to the patients' age.
Serotonin, osteocalcin, procollagen type-1 aminoterminal propeptide, and
beta-isomerized C-terminal cross-linked peptide of collagen type I were much
lower in diabetic hemodialysis patients.
CONCLUSIONS: Serotonin may increase both bone formation and bone resorption in
hemodialysis patients. The reverse relation of serotonin to patients' age as well
as its lower levels in diabetic hemodialysis patients indicate that low plasma
serotonin may contribute to the higher incidence of low-turnover bone disease
that characterizes old and diabetic hemodialysis patients.

Am J Physiol Endocrinol Metab. 2012 Apr 15;302(8):E1009-15.
Mammary gland serotonin regulates parathyroid hormone-related protein and other
bone-related signals.
Hernandez LL(1), Gregerson KA, Horseman ND.
(1)Department of Molecular and Cellular Physiology, University of Cincinnati,
Cincinnati, Ohio, USA.
Breast cells drive bone demineralization during lactation and metastatic cancers.
A shared mechanism among these physiological and pathological states is endocrine
secretion of parathyroid hormone-related protein (PTHrP), which acts through
osteoblasts to stimulate osteoclastic bone demineralization. The regulation of
PTHrP has not been accounted for fully by any conventional mammotropic stimuli or
tumor growth factors. Serotonin (5-HT) synthesis within breast epithelial cells
is induced during lactation and in advancing breast cancer. Here we report that
serotonin deficiency (knockout of tryptophan hydroxylase-1) results in a
reduction of mammary PTHrP expression during lactation, which is rescued by
restoring 5-HT synthesis. 5-HT induced PTHrP expression in lactogen-primed
mammary epithelial cells from either mouse or cow. In human breast cancer cells
5-HT induced both PTHrP and the metastasis-associated transcription factor
Runx2/Cbfa1. Based on receptor expression and pharmacological evidence, the 5-HT2
receptor type was implicated as being critical for induction of PTHrP and Runx2.
These results connect 5-HT synthesis to the induction of bone-regulating factors
in the normal mammary gland and in breast cancer cells.

 

[Bumberleybee]

Would a cortisol test now (28 yrs after diagnosis of type one diabetes) be of any use? What might it show and how might it help me work things out?

It could show whether it’s chronically high. It can help to judge the doses of the things that lower it—pregnenolone, progesterone, aspirin, sugar, thyroid, calcium, etc.

 

[Bumberleybee]

Dear Ray,

With type one diabetes, what foods would you recommend, if dairy cannot currently be eaten, to ensure bowel movements? I understand milk provides bulk.

Is commercial pasteurised not from concentrate orange juice okay as the staple of my diet?

And should potatoes be avoided altogether with type one diabetes, if they are likely to increase endotoxins, or are they okay if baked and topped with butter and salt?

Have you tried various cheeses? Orange juice is good, though the quality of the commercial products varies. Some people do well with well-cooked potatoes with butter, but the condition of the intestine affects the reaction. A daily raw carrot is sometimes enough to disinfect the intestine.

No cheese as yet, I'm getting married next month so wanted to avoid risking the acne dairy causes me until after then. Which cheeses are best to start with please?

I tried eggshells tonight, I was wondering how much eggshell is recommended to get enough calcium each day please? I had 1 whole eggshell tonight.

Tillamook vintage white sharp cheddar (2 or 3 years aged), Parmigiano reggiano, and pecorino romano are currently the safest. The Tillamook cheese process has been changed, so only what’s currently aging has the traditional composition.

 

[Ashoka]

[moderator edit: shared by Ashoka, copied from https://raypeatforum.com/community/threads/what-can-one-do-about-a-hiatal-hernia.7629/#post-120486]


Peat's responded to me months ago in two emails, which I'm providing as a resource for others:

Me:

"Hi Dr. Peat,

I have a hiatal hernia that causes chest pains, chest and throat tightness, shallow breathing, occasional palpitations, constant heartburn, bloating, asthma-like symptoms, and other things. I went to the ER for the chest pains and it was judged as "non-cardiac" in origin. When hiatal hernia is suspected, general medicine doesn't offer an approach to recovery beyond symptom management or surgery.

Is there anything to do for a hiatal hernia? For example, some chiropractors claim to be able to treat it. It seems this is a prevalent and dangerous illness and people have no idea how to approach it."

Peat:

"Have you had blood tests for hormones? The whole complex of symptoms including hiatal hernia is usually caused by a general weakness of digestive and hormonal processes, and it’s especaily imortant to check thyroid function carefully, with a blood test and recording waking and midday temperature and pulse rate, and average caloric requirement."

Me:

"Hi again Dr. Peat,

I had blood tests for hormones a couple of times about a year ago. I first started struggling with my health after taking the drug finasteride for two months. When I stopped the drug, almost overnight I developed low libido, brain fog, and fatigue. A year and a half since, I've started feeling slightly better but recently developed this HH. I find it difficult to eat to caloric needs due to the HH."

Peat:

"It is most likely to develop as a result of reduced thyroid hormone and increased stress hormones (especially cortisol, in relation to testosterone and DHEA), weakening connective tissues. Some foods that cause intestinal irritation can make it worse; a simplified diet makes it possible to identify any specific foods that make the problem worse. Keeping a record of temperature and pulse rate can help to recognize any hormonal problems."

 

[James_001]

Dr. Peat,

I was wondering if you could recommend a brand of t3 only medication now that cytomel is out of production?

Thank you

The only other one that I’ve tried was Pro T3 from Anti-aging systems.

Dr. Peat,

I was wondering if you would have any ideas as to why someone would expereince a complete alleviation of hypothyroid symptoms for one week taking a combination of synthetic t3 and t4, yet follow the first week experience a reversion back to a hypothyroid state despite the same dose of thyroid being consumed?

Assuming this person's diet is good, and pulse and temps are optimal on the thyroid medication.

Thanks you so much, Jake

During the first week or two of supplementing thyroid, there is usually an intensification of the effect of adrenaline. It’s necessary to watch a variety of signs, especially the temperature of hands and feet and the amount of water evaporated, to judge the actual effect of thyroid. The effect of thyroid after the level of adrenaline has normalized is to increase the depth of relaxation.

During the first week or two of supplementing thyroid, there is usually an intensification of the effect of adrenaline. It’s necessary to watch a variety of signs, especially the temperature of hands and feet and the amount of water evaporated, to judge the actual effect of thyroid. The effect of thyroid after the level of adrenaline has normalized is to increase the depth of relaxation.

Dr. Peat,

What do you think of testosterone injections for someone whose thyroid function is good, but still has issues raising testosterone levels? Assuming that dhea and pregnenolone have already been used.

Do you think that gels or creams are superior to injections?

Thank you

I think an oil or cream with real testosterone (and DHEA) is much better than the injections, which are usually an ester of testosterone in a toxic solvent.

I think an oil or cream with real testosterone (and DHEA) is much better than the injections, which are usually an ester of testosterone in a toxic solvent.

Hey Dr. Peat,

I recently made an observation that I wanted to ask you about.

I am a mathematics student at university and I often find that mathematics professors are authoritative and tend to put down students for getting an incorrect answer.

It seems like they do not like questions very much, on the other hand the humanities professors seem more open to student involvement and questioning.

Do you think that this is a product off the culture that mathematicians are involved in?

Or is it a result of mathematical rigid thinking that changes the structure of their brain away from analogous thinking to logical thinking?

Or both?

I was thinking that people choose mathematics as a professor because they want to maintain an illusion of certainty in their minds, which stands in opposition to questioning and exploration.

I also think that the repetitive, monotonous calculations might be related to serotonin levels somehow, and as a result hostility and aggression?

What do you think?

thanks, Jake

Your comments and suggestions are so insightful, I’m surprised to hear that you’re a math student. I think the serotonin aspect is involved, with “inescapable stress” a part of the culture. (For rats, biting the source of the stress is therapeutic.) I think a profession attracts people with a certain personality type, and then reinforces certain traits and biochemical balances. All of the mathematicians that I’ve known held a platonist view of math, that affected their general mentality—an avoidance of ambiguity and perceptual richness, an inflexibility or authoritarianism in everything. Alfred North Whitehead was a mathematician who very successfully got out of the platonist culture/personality; he recognized that the body is always a part of the cognitive processes.

 

[goodandevil]

Dr. Peat,

I have severe pelvic floor dysfunction, with sometimes static digestion. I've relied on marijuana to sleep and control my restless leg. Every time I stop marijuana, I have quite severe pupil dilation, sweating, and piloerection. Also, I have very apparent veins in the palms of my hand and blotchy hand skin.

T4 helped me initially (12 mcg), but I suffered from eye pain, worsening restless legs, and very dry skin. I switched to T3. Though T3 felt very good, on it I was plagued with eye infections, rather than eye pain, and very dry nostrils.

Despite the cortisol reaction to t4, might it still benefit me to combine the t4 with t3? Might the pupil dilation indicate pituitary damage, perhaps secondary to the marijuana?

Most Respectfully Yours,

James

RAY PEAT REPLIES:

"Adrenaline can increase to compensate for low thyroid function, and causes pupils to dilate. Thyroxin by itself works when your liver is in good condition, supplied with enough glucose, and not stressed by adrenaline and other stress hormones. Something that contains both T4 and T3 is better for getting out of a stress pattern. Armour thyroid or Novotiral might work better than Eutirox. Too much of the weed interferes with liver function, and while it’s recovering it’s necessary to be careful to get enough protein and other nutrients every day, for example orange juice, eggs, milk, cheese, cooked mushrooms, occasional shellfish."

 

[goodandevil]

"For about a month, I took 30-40k IUs daily vitamin a. Might that account for some eye troubles and very dry skin? I read a chinese paper that taurine and zinc help hypervitaminosis a, do you know of anything else, and would transthyretin saturation by A interfere with supplemental t4? As with all of us, i appreciate your dedication and humanity ineffably."

Ray:
"Vitamin A oxidizes easily and an excess can create symptoms of a deficiency, so vitamin E is the most important thing for correcting it; excess vitamin A, like PUFA, interferes with thyroid hormone transport, so it’s important to balance the two."

 

[Lightbringer]

I recently found a milk brand called <xyz> lactose free 2% fat milk. This contains less than 1% of Lactase enzyme. Is this safe to consume in your opinion ?

I think the lactase milk is safe.

 

[Sheila]

Question was regarding a 14yo boy born with a brain injury, with respect to what also might improve his brain function to enable talking. Recent introduction of 're-breathing' has reduced his spasmic movements, quietened his brain and may have improved his very dry skin. His temps are 36-37 but pulse very difficult to find. Also his brain is slowed (in a helpful way) when he eats (if rarely) nori rolls of salmon, avocado, sushi rice and seaweed surround. His general diet is excellent, digestible, low PUFA/gluten, sufficient etc. so the effect of this 'meal' is interesting. Slowing down "my brain firing too much" as he tells us, should help, does anything else occur to you [Dr Peat] that we could try?

Dr Peat kindly replies:

The dry skin and weak pulse suggest very low thyroid function. The salmon, avocado, and rice are a good balance of fat, protein, and carbohydrate; maybe fat cheese could be substituted for the salmon sometimes. Both sugar and fat stimulate the digestive system hormone that stimulates brain cell renewal. Progesterone helps to reduce tension and excitation, and protects nerves. Pregnenolone reduces stress, and protects nerves.

J Neurosci. 2005 Feb 16;25(7):1816-25.

Glucose-dependent insulinotropic polypeptide is expressed in adult hippocampus and induces progenitor cell proliferation.

Nyberg J(1), Anderson MF, Meister B, Alborn AM, Ström AK, Brederlau A, Illerskog
AC, Nilsson O, Kieffer TJ, Hietala MA, Ricksten A, Eriksson PS.
(1)The Arvid Carlsson Institute for Neuroscience at the Institute of Clinical
Neuroscience, Göteborg University, Sahlgrenska University Hospital, 413 45
Göteborg, Sweden. [email protected]

The hippocampal dentate gyrus (DG) is an area of active proliferation and
neurogenesis within the adult brain. The molecular events controlling adult cell
genesis in the hippocampus essentially remain unknown. It has been reported
previously that adult male and female rats from the strains Sprague Dawley (SD)
and spontaneously hypertensive (SHR) have a marked difference in proliferation
rates of cells in the hippocampal DG. To exploit this natural variability and
identify potential regulators of cell genesis in the hippocampus, hippocampal
gene expression from male SHR as well as male and female SD rats was analyzed
using a cDNA array strategy. Hippocampal expression of the gene-encoding
glucose-dependent insulinotropic polypeptide (GIP) varied strongly in parallel
with cell-proliferation rates in the adult rat DG. Moreover, robust GIP
immunoreactivity could be detected in the DG. The GIP receptor is expressed by
cultured adult hippocampal progenitors and throughout the granule cell layer of
the DG, including progenitor cells. Thus, these cells have the ability to respond
to GIP. Indeed, exogenously delivered GIP induced proliferation of adult-derived
hippocampal progenitors in vivo as well as in vitro, and adult GIP receptor
knock-out mice exhibit a significantly lower number of newborn cells in the
hippocampal DG compared with wild-type mice. This investigation demonstrates the
presence of GIP in the brain for the first time and provides evidence for a
regulatory function for GIP in progenitor cell proliferation.


Mol Cell Neurosci. 2005 Jul;29(3):414-26.
Thyroid hormone regulates hippocampal neurogenesis in the adult rat brain.
Desouza LA(1), Ladiwala U, Daniel SM, Agashe S, Vaidya RA, Vaidya VA.

(1)Department of Biological Sciences, Tata Institute of Fundamental Research,
Mumbai 400005, India.

We have examined the influence of thyroid hormone on adult hippocampal
neurogenesis, which encompasses the proliferation, survival and differentiation
of dentate granule cell progenitors. Using bromodeoxyuridine (BrdU), we
demonstrate that adult-onset hypothyroidism significantly decreases hippocampal
neurogenesis. This decline is predominantly the consequence of a significant
decrease in the survival and neuronal differentiation of BrdU-positive cells.
Both the decreased survival and neuronal differentiation of hippocampal
progenitors could be rescued by restored euthyroid status. Adult-onset
hyperthyroidism did not influence hippocampal neurogenesis, suggesting that the
effects of thyroid hormone may be optimally permissive at euthyroid levels. Our
in vivo and in vitro results revealed that adult hippocampal progenitors express
thyroid receptor isoforms. The in vitro studies demonstrate that adult
hippocampal progenitors exhibit enhanced proliferation, survival and glial
differentiation in response to thyroid hormone. These results support a role for
thyroid hormone in the regulation of adult hippocampal neurogenesis and raise the
possibility that altered neurogenesis may contribute to the cognitive and
behavioral deficits associated with adult-onset hypothyroidism.

Nutr Res. 2014 Aug;34(8):653-60.

High saturated fatty acid intake induces insulin secretion by elevating gastric
inhibitory polypeptide levels in healthy individuals.
Itoh K(1), Moriguchi R(2), Yamada Y(3), Fujita M(4), Yamato T(2), Oumi M(2),
Holst JJ(5), Seino Y(6).

(1)Faculty of Nutritional Sciences, Nakamura Gakuen University, Fukuoka, Japan.
Electronic address: [email protected]. (2)Faculty of Nutritional Sciences,
Nakamura Gakuen University, Fukuoka, Japan. (3)Department of Internal Medicine,

Akita University, Akita City, Japan. (4)Department of Public Health, Chiba
University, Chiba, Japan. (5)Department of Biomedical Sciences, Panum Institute,
University of Copenhagen, Copenhagen, Denmark. (6)Kansai Electric Power Hospital,
Osaka, Japan.

Insulin resistance is central to the etiology of the metabolic syndrome cluster
of diseases. Evidence suggests that a high-fat diet is associated with insulin
resistance, which may be modulated by dietary fatty acid composition. We
hypothesized that high saturated fatty acid intake increases insulin and gastric
inhibitory polypeptide (GIP) secretion. To clarify the effect of ingested fatty
acid composition on glucose levels, we conducted an intervention study to
investigate the insulin and plasma GIP responses in 11 healthy women, including a
dietary control. Subjects were provided daily control meals (F-20; saturated
fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P]
ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental
meals for 7 days each. These meals comprised 60 E% carbohydrate, 15 E% protein,
and 30 E% fat (FB-30; high saturated fatty acid meal; S/M/P, 5:4:1; F-30: reduced
saturated fatty acid meal; S/M/P, 3:4:3). On the second day of the F-20 and the
last day of F-30 and FB-30, blood samples were taken before and 30, 60, and 120
minutes after a meal tolerance test. The plasma glucose responses did not differ
between F-20 and FB-30 or F-30. However, insulin levels were higher after the
FB-30 than after the F-20 (P < .01). The GIP response after the FB-30 was higher
than that after the F-30 (P < .05). In addition, the difference in the
incremental GIP between FB-30 and F-30 correlated significantly and positively
with that of the insulin. These results suggest that a high saturated fatty acid
content stimulates postprandial insulin release via increased GIP secretion.
Copyright © 2014 Elsevier Inc. All rights reserved.



Gene. 2010 Sep 1;463(1-2):29-40.
Functional identification of an intronic promoter of the human glucose-dependent
insulinotropic polypeptide gene.

Hoo RL(1), Chu JY, Yuan Y, Yeung CM, Chan KY, Chow BK.
(1)School of Biological Sciences, The University of Hong Kong, Hong Kong SAR, PR
China.

Glucose-dependent insulinotropic polypeptide (GIP), a physiological incretin and
enterogastrone, plays a vital role in regulating glucose-dependent insulin
release from the pancreas and gastric acid secretion from the stomach. By using a
transgenic mouse approach, we previously reported that the distal 1.2kb promoter
region of the human GIP (hGIP) gene (-2545/-346, relative to the ATG) was able to
target the transgene expression in the stomach but not in the small intestine
where the majority of GIP-producing cells are located. In the present study, in
order to identify the cis-acting element(s) that is/are required for intestinal
expression, a 1.6kb (-1580/-) DNA fragment within the first intron of the hGIP
gene was isolated and characterized in three GIP-expressing cell lines including
HuTu80 (duodenal cells), PANC-1 (pancreatic ductal cells) and Hs746T (stomach
cells). By 5' and 3' deletion analysis, a proximal promoter element was confined
within the nucleotides -102/-1. This promoter element, functions in an
orientation-dependent manner, was able to drive 15.1 and 18.3 fold increases in
promoter activities in HuTu80 and PANC-1 cells, respectively. Site-directed
mutation analysis indicated that the region -54/-23 was essential for promoter
function while the region -22/-1 might possess opposite effects in HuTu80 and

PANC-1 cells. In competitive and antibody supershift assays, interactions of the
progesterone receptor (PR) and some unknown protein factors from HuTu80 and
PANC-1 with the motif(s) at -54/-23 were evident. Consistent with this finding,
we demonstrated the transcriptional regulation of the hGIP promoter by
progesterone via the PR-B isoform and that progesterone treatment in both HuTu80
and PANC-1 cells resulted in an increase in hGIP transcript level. In addition, a
sequence motif (ACATGT) residing -48/-43 was found to be responsible for the
binding of potential TFII regulator(s). Taken together, our results suggest that
the proximal intronic sequences contain essential cis-acting elements for the
cell-specific expression of the hGIP gene.

Copyright 2010 Elsevier B.V. All rights reserved.


J Am Coll Nutr. 2009 Jun;28(3):286-95.
The degree of saturation of fatty acids in dietary fats does not affect the
metabolic response to ingested carbohydrate.
Radulescu A(1), Hassan Y, Gannon MC, Nuttall FQ.

(1)Endocrine, Metabolism and Nutrition Section (111G), VA Medical Center,
Minneapolis, MN 55417, USA.

BACKGROUND: We are interested in the metabolic response to ingested
macronutrients, and the interaction between macronutrients in meals. Previously,
we and others reported that the postprandial rise in serum glucose following
ingestion of 50 g carbohydrate, consumed as potato, was markedly attenuated when
butter was ingested with the carbohydrate, whereas the serum insulin response was
little affected by the combination.

OBJECTIVE: To determine whether a similar response would be observed with three
other dietary fats considerably different in fatty acid composition.
DESIGN: Nine healthy subjects received lard, twelve received olive oil and eleven
received safflower oil as a test meal. The subjects ingested meals of 25 g fat
(lard, olive oil or safflower oil), 50 g CHO (potato), 25 g fat with 50 g CHO or
water only. Glucose, C peptide, insulin, triacylglycerols and nonesterified fatty
acids were determined.

RESULTS: Ingestion of lard, olive oil or safflower oil with potato did not affect
the quantitative glucose and insulin responses to potato alone. However, the
responses were delayed, diminished and prolonged. All three fats when ingested
alone modestly increased the insulin concentration when compared to ingestion of
water alone. When either lard, olive oil or safflower oil was ingested with the
potato, there was an accelerated rise in triacylglycerols. This was most dramatic
with safflower oil.

CONCLUSIONS: Our data indicate that the glucose and insulin response to butter is
unique when compared with the three other fat sources varying in their fatty acid
composition.

...........

[ moderator edit: related thread RP Email Advice Discussion: Salmon, Avocado And Rice ]

 

[milk_lover]

I asked Dr Peat about Lysine supplementation and I got an answer :)

My question:
I know you’re not a big fan of individual amino acid supplementation, but if we assume we have a pure source of L-lysine, is it a wise decision to take it daily for its benefits on opposing gut serotonin and NO?

Dr Peat's answer:
If its use relieves symptoms, it should be safe, but I think there’s always some risk with manufactured amino acids. Taking it with a meal would reduce risk of inflammation.