Hi,
My brother is of 14 and 6 months ago detected with type 1. Recently I heard about "Insulin Plants".
My questions are
Will it help in type 1 diabetes ?
How to use it ?
Do he needs to take it lifelong?
Any side-effects of it ?
Insulin plant for type 1 diabetes - Diabetes India
Insulin plant for type 1 diabetes
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RiddhiGohil
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39 Replies
β’
Type1 diabetes could get a good result ina meal of high proteins and high carbs almost in 50 /50 ratio. Try that under the supervision of a doctor who concedes this point , which is almost impossible, because of their mental make up.
That's why with supervision . That diet of high carb and high protein means not unlimited food , but with in the stipulated and allowed calories . When a diet of 60 percent fats , even if good fats , is not dangerous how can this be dangerous . only high protein meal is dangerous for kidneys . Only high carb could be dangerous in the threat of sugar problems . But when both are taken insulin and glucagon may counter balance each other .Any way it is a suggestion and can be implemented only with the care and advise of a doctor .It is not any synthetic drug or injection . Just ordinary food which other members of the family take. Constant and continuous monitoring does not give any threat . OK , that is over .
β’ in reply to
Carbs mean not junk food . Proteins mean not from junk food . Carbs from whole grains and mixed grains , proteins from plant sources seeds like water melon , musk melon , pumpkin , til seeds ,chick peas , kabuli chana etc and turdal , green gram dal , bengal gram dal etc . Even cooking with minimum oil that also derived from plant sources . Carbs and proteins in equal proportions and the whole intake in the allowable limit of calories . This food ---- we experimented and found out . This is not unscientific fare dished out from quacks .Ghee was recommended in the olden days . But not now since the quality is highly questionable .Even the quality of milk is not good now a days .Vegetables like cabbage , lauki , thinda , carrots , clusterbeans , even greens which are in great demand are highly toxic with chemicals because of the profit motive . Fruits are no exception . This is the present scenario in India .Since we have to eat something we are helpless. In such situation the calories concept can't be thrown out and indiscriminate eating leads to more and more diseases for which again new names and new medicines are given .
Hidden
"Carbs mean not junk food". Not for D people. We can't utilize glucose efficiently. So we should avoid. There are other sources of energy.
"Cooking with minimum oil that also derived from plant sources".
Why minimal oil?
"That's why with supervision. That diet of high carb and high protein means not unlimited food, but with in the stipulated and allowed calories. When a diet of 60 percent fats, even if good fats, is not dangerous how can this be dangerous". Please explain how are fats dangerous?
You are on a wrong path totally. Yes a little more protein is required say 1g / kg / day for this boy of 14, but he needs to restrict carbs.
Hidden
"That's why with supervision ". Please be specific. What kind of supervision exacty?
Insulin and glucagon are always counter balanced. How does high carb high protein diet would do that?
"Just ordinary food which other members of the family take. Constant and continuous monitoring does not give any threat ". It's ordinary food - carbs that is harmful to us. Constant monitoring will give you information but will not solve the problem. You will have to resort to synthetic drugs and injections if you find high bs readings.
β’ in reply tosuramo
If it is found out that the experiment is not giving expected results after a period of 2 months it can be stopped and could be reverted back to the other options .Even before that time stipulated if any damage is observed it can be stopped . Any method takes the first trial before being followed . That includes high fats also.One size does not fit all and in case of diabetes no standard rule is applicable to all .
Hidden
"If it is found out that the experiment is not giving expected results...". Sorry. No experiments, please. Why not to start with what is scientific? I don't understand why you want to give something -carb - which is harmful to D people. Good Fats are not harmful.
β’ in reply tosuramo
What is scientific ? It is not medicine . It is ordinary simple home cooked food . Just as you believe a theory we do believe . In the first instance yours' was also a opinion , then it became a theory , then it became SCIENCE according to you . Hats off .Any way when somebody follows that diet and experience the results they would decide whether to go go ahead or not .At some time . some where , some body experimented with your diet theory . So please leave the issue here . ,
β’ in reply to
What is science ?Many times the scientific research goes back on their findings .Not long back Metformin was praised to sky saying that it was very good in diabetic medications .Now a recent studu found out that the use of Metformin in people with diabetes increased the risk of dementia and Parkinson's disease. One reason could be according to them , the contribution of Metformin to the decrease in B12 deficiency . Of course that point is not yet confirmed .We all know that B12 DEFICIENCY leads to neurological problems and nerve damage . Here my point is Science is not giving any foolproof solution and it is always better to go for time tested methods , whether in food or rest or medicine.Carbs entering the small intestines are broken in tomonosacharides and proteins in the duodenum are turned in to amino acids .A judicious balance of both could reduce the bad effects of insulin deficiency in case of type 1 diabetes . Since it is natural process it is better to go for the diet cooked at home and that also under calorie control . The arguments are not exhausted ,but I want to put a stop to this battle of words from my side .Time will reveal the harms of high fat diet .For any thing to be proved minimum period of 12 years is required . Till such time the field is free for tirade for some .
Hidden
"Carbs entering the small intestines are broken in tomonosacharides and proteins in the duodenum are turned in to amino acids .A judicious balance of both could reduce the bad effects of insulin deficiency in case of type 1 diabetes . "
How ? I don't see any logic or science. Carbs and protein both need insulin to get cleared from blood. Do you wear a footwear that doesn't fit you ? Do you drink freeze water if it causes common cold or sore throat to you ? Why do you want to give high carb diet and more insulin dosage to that type 1 child ? It's a misfit diet.
All veg people whether D or not have deficiency of b12. But in D b12 demand increases to combat and get rid of neuronal effects.
"For any thing to be proved minimum period of 12 years is required "
Is there any logic / science in postulating 12 year period ? It's much sooner than you say. Perhaps less than a year. If as you say fats are bad anup who is on high fat diet for 7 years would have faced at least a few complications π
"Time will reveal the harms of high fat diet ". But the time has already revealed the harms of high carb diet.
Do you know high protein diet upregulates mTor system, the system which is responsible for cell division and growth. Thought to be causing cancer and ageing, this mTor.
Clinical significance
Aging
mTOR signaling pathway.[1]
Decreased TOR activity has been found to increase life span in S. cerevisiae, C. elegans, and D. melanogaster.[52][53][54][55] The mTOR inhibitor rapamycin has been confirmed to increase lifespan in mice.[56][57][58][59][60]
It is hypothesized that some dietary regimes, like caloric restriction and methionine restriction, cause lifespan extension by decreasing mTOR activity.[52][53] Some studies have suggested that mTOR signaling may increase during aging, at least in specific tissues like adipose tissue, and rapamycin may act in part by blocking this increase.[61] An alternative theory is mTOR signaling is an example of antagonistic pleiotropy, and while high mTOR signaling is good during early life, it is maintained at an inappropriately high level in old age. CR and methionine restriction may act in part by limiting levels of essential amino acids including leucine and methionine, which are potent activators of mTOR.[62] The administration of leucine into the rat brain has been shown to decrease food intake and body weight via activation of the mTOR pathway in the hypothalamus.[63]
According to the free radical theory of aging,[64] reactive oxygen species cause damage of mitochondrial proteins and decrease ATP production. Subsequently, via ATP sensitive AMPK, the mTOR pathway is inhibited and ATP consuming protein synthesis is downregulated, since mTORC1 initiates a phosphorylation cascade activating the ribosome.[14] Hence, the proportion of damaged proteins is enhanced. Moreover, disruption of mTORC1 directly inhibits mitochondrial respiration.[65] These positive feedbacks on the aging process are counteracted by protective mechanisms: Decreased mTOR activity (among other factors) upregulates glycolysis[65] and removal of dysfunctional cellular components via autophagy.[64]
Brain functionEdit
CancerEdit
Over-activation of mTOR signaling significantly contributes to the initiation and development of tumors and mTOR activity was found to be deregulated in many types of cancer including breast, prostate, lung, melanoma, bladder, brain, and renal carcinomas.[66] Reasons for constitutive activation are several. Among the most common are mutations in tumor suppressor PTEN gene. PTEN phosphatase negatively affects mTOR signalling through interfering with the effect of PI3K, an upstream effector of mTOR. Additionally, mTOR activity is deregulated in many cancers as a result of increased activity of PI3K or Akt.[67] Similarly, overexpression of downstream mTOR effectors 4E-BP1, S6K and eIF4E leads to poor cancer prognosis.[68] Also, mutations in TSC protein that inhibits the activity of mTOR may lead to a condition named tuberous sclerosis complex, which exhibits as benign lesions and increases the risk of renal cell carcinoma.[69]
Increasing mTOR activity was shown to drive cell cycle progression and increase cell proliferation mainly thanks to its effect on protein synthesis. Moreover, active mTOR supports tumor growth also indirectly by inhibiting autophagy.[70] Constitutively activated mTOR functions in supplying carcinoma cells with oxygen and nutrients by increasing the translation of HIF1A and supporting angiogenesis.[71] mTOR also aids in another metabolic adaptation of cancerous cells to support their increased growth rate - activation of glycolytic metabolism. Akt2, a substrate of mTOR, specifically of mTORC2, upregulates expression of the glycolytic enzyme PKM2 thus contributing to the Warburg effect.[72]
Central nervous system disordersEdit
Main article: Central nervous system disorder
AutismEdit
MTOR is implicated in the failure of a 'pruning' mechanism of the excitatory synapses in autism spectrum disorders.[73]
Alzheimerβs diseaseEdit
mTOR signaling intersects with Alzheimerβs disease (AD) pathology in several aspects, suggesting its potential role as a contributor to disease progression. In general, findings demonstrate mTOR signaling hyperactivity in AD brains. For example, postmortem studies of human AD brain reveal dysregulation in PTEN, Akt, S6K, and mTOR.[74][75][76] mTOR signaling appears to be closely related to the presence of soluble amyloid beta (AΞ²) and tau proteins, which aggregate and form two hallmarks of the disease, AΞ² plaques and neurofibrillary tangles, respectively.[77] In vitro studies have shown AΞ² to be an activator of the PI3K/AKT pathway, which in turn activates mTOR.[78] In addition, applying AΞ² to N2K cells increases the expression of p70S6K, a downstream target of mTOR known to have higher expression in neurons that eventually develop neurofibrillary tangles.[79][80] Chinese hamster ovary cells transfected with the 7PA2 familial AD mutation also exhibit increased mTOR activity compared to controls, and the hyperactivity is blocked using a gamma-secretase inhibitor.[81][82] These in vitro studies suggest that increasing AΞ² concentrations increases mTOR signaling; however, significantly large, cytotoxic AΞ² concentrations are thought to decrease mTOR signaling.[83]
Consistent with data observed in vitro, mTOR activity and activated p70S6K have been shown to be significantly increased in the cortex and hippocampus of animal models of AD compared to controls.[82][84] Pharmacologic or genetic removal of the AΞ² in animal models of AD eliminates the disruption in normal mTOR activity, pointing to the direct involvement of AΞ² in mTOR signaling.[84] In addition, by injecting AΞ² oligomers into the hippocampi of normal mice, mTOR hyperactivity is observed.[84] Cognitive impairments characteristic of AD appear to be mediated by the phosphorylation of PRAS-40, which detaches from and allows for the mTOR hyperactivity when it is phosphorylated; inhibiting PRAS-40 phosphorylation prevents AΞ²-induced mTOR hyperactivity.[84][85][86] Given these findings, the mTOR signaling pathway appears to be one mechanism of AΞ²-induced toxicity in AD.
The hyperphosphorylation of tau proteins into neurofibrillary tangles is one hallmark of AD. p70S6K activation has been shown to promote tangle formation as well as mTOR hyperactivity through increased phosphorylation and reduced dephosphorylation.[79][87][88][89] It has also been proposed that mTOR contributes to tau pathology by increasing the translation of tau and other proteins.[90]
Synaptic plasticity is a key contributor to learning and memory, two processes that are severely impaired in AD patients. Translational control, or the maintenance of protein homeostasis, has been shown to be essential for neural plasticity and is regulated by mTOR.[82][91][92][93][94] Both protein over- and under-production via mTOR activity seem to contribute to impaired learning and memory. Furthermore, given that deficits resulting from mTOR overactivity can be alleviated through treatment with rapamycin, it is possible that mTOR plays an important role in affecting cognitive functioning through synaptic plasticity.[78][95] Further evidence for mTOR activity in neurodegeneration comes from recent findings demonstrating that eIF2Ξ±-P, an upstream target of the mTOR pathway, mediates cell death in prion diseases through sustained translational inhibition.[96]
Some evidence points to mTORβs role in reduced AΞ² clearance as well. mTOR is a negative regulator of autophagy;[97] therefore, hyperactivity in mTOR signaling should reduce AΞ² clearance in the AD brain. Disruptions in autophagy may be a potential source of pathogenesis in protein misfolding diseases, including AD.[98][99][100][101][102][103] Studies using mouse models of Huntingtonβs disease demonstrate that treatment with rapamycin facilitates the clearance of huntingtin aggregates.[104][105] Perhaps the same treatment may be useful in clearing AΞ² deposits as well.
Protein synthesis and cell growthEdit
mTORC1 activation is required for myofibrillar muscle protein synthesis and skeletal muscle hypertrophy in humans in response to both physical exercise and ingestion of certain amino acids or amino acid derivatives.[106][107] Persistent inactivation of mTORC1 signaling in skeletal muscle facilitates the loss of muscle mass and strength during muscle wasting in old age, cancer cachexia, and muscle atrophy from physical inactivity.[106][107][108] mTORC2 activation appears to mediate neurite outgrowth in differentiated mouse neuro2a cells.[109] Intermittent mTOR activation in prefrontal neurons by Ξ²-hydroxy Ξ²-methylbutyrate inhibits age-related cognitive decline associated with dendritic pruning in animals, which is a phenomenon also observed in humans.[110]
Signaling cascade diagram
Diagram of the molecular signaling cascades that are involved in myofibrillar muscle protein synthesis and mitochondrial biogenesis in response to physical exercise and specific amino acids or their derivatives (primarily leucine and HMB).[106] Many amino acids derived from food protein promote the activation of mTORC1 and increase protein synthesis by signaling through Rag GTPases.[8][106]
Abbreviations and representations:
β’ PLD: phospholipase D
β’ PA: phosphatidic acid
β’ mTOR: mechanistic target of rapamycin
β’ AMP: adenosine monophosphate
β’ ATP: adenosine triphosphate
β’ AMPK: AMP-activated protein kinase
β’ PGCβ1Ξ±: peroxisome proliferator-activated receptor gamma coactivator-1Ξ±
β’ S6K1: p70S6 kinase
β’ 4EBP1: eukaryotic translation initiation factor 4E-binding protein 1
β’ eIF4E: eukaryotic translation initiation factor 4E
β’ RPS6: ribosomal protein S6
β’ eEF2: eukaryotic elongation factor 2
β’ RE: resistance exercise; EE: endurance exercise
β’ Myo: myofibrillar; Mito: mitochondrial
β’ AA: amino acids
β’ HMB: Ξ²-hydroxy Ξ²-methylbutyric acid
β’ β represents activation
β’ Ξ€ represents inhibition
Graph of muscle protein synthesis vs time
Resistance training stimulates muscle protein synthesis (MPS) for a period of up to 48 hours following exercise (shown by dotted line).[111] Ingestion of a protein-rich meal at any point during this period will augment the exercise-induced increase in muscle protein synthesis (shown by solid lines).[111]
SclerodermaEdit
Scleroderma, also known as systemic sclerosis, is a chronic systemic autoimmune disease characterised by hardening (sclero) of the skin (derma) that affects internal organs in its more severe forms.[112][113] mTOR plays a role in fibrotic diseases and autoimmunity, and blockade of the mTORC pathway is under investigation as a treatment for scleroderma.[7]
β’ in reply tosuramo
So all people of 60% fats are absolutely free from diabetes since they are under that diet for the past 4 years as per their version .
Hidden
They are drugfree. Control / reversed their D by strictly avoiding carbs as much as possible. The defect regarding carb doesn't go away lifetime. You have to avoid what's harmful. It's like taming a wild dog ππππ
β’ in reply tosuramo
I have been insisting on moderation and I do stick to my argument that excess of any thing is bad . So I repeatedly said calorie restriction .Equal portions of carbs and proteins do not mean unlimited portions . In the limited allowance ------equal portions . Any way fats come from sources such as nuts like sesame , ground nuts , etc and milk products also . Along with that limited oil used in seasoning and cooking is sufficient for the need of fats .Let us see after 5 years the result of the arguments from both sides .
Hidden
ππππ.
"So I repeatedly said calorie restrictions "
Well in general that is true but not for the child (or any child) we are talking about. They need extra calorie and extra protein for their physical (and mental ) growth.
"...limited oil used in seasoning and cooking is sufficient for the need of fats.."
Can we know in which proportion do you recommend c : p : f ?
" Let us see after 5 years the result of the arguments from both sides" πππππ. 5 years are very vital for this child. What would you advise to avoid adverse effects of high bs by that time ? Insulin π³π³πππ. But that will increase fat deposition in the body and would increase ir. That child may become fatty and metabolically deranged π³π³ππ.
No madam. No no to the discussion. Let us argue out the matter here. If i'm wrong i'd apologize. Let us all know your viewpoints. Tell us all exacty how much carb, protein and fats he should be given.
By the way any oil that contains mufa and pufa is not good for cooking. Heat oxidises such oils. Such oils include peanut, sesame mastard etc oils. Further only kachchi ghani oil are to be used. Any rbd oil should be thrown into garbage. I recommend co vco and ghee for cooking and evoo for dressing.
I'm eager to learn from you
β’ in reply tosuramo
Assuming that a 14 year old child needs some 2 400 calories per day for the healthy growth 1000 calories could be given in carbs and 1000 calories in proteins and 400 in the form of fats . The 1000 calories in carbs and 1000 calories in proteins can be divided in to 3 medium sized meals and 3 in between niblings ----- one fruit along with breakfast , one chacolate in the recess period in the school , one laddu made of groundnuts or sesame seeds or some sweet made up of carbs and proteins in the evening . Carbs include the carbs of vegetables and greens . Proteins include yogurt , nuts and other material depending upon their food type . According to my observation this division would not give sugar spikes in volatile ways . Each individual case has to be dealt in a different way and in the initial stages may require caloric counting and the performance . Once the routine is established , the caloric values of different foods are known , there is no need to do daily calculations .Out of the 2400 calories need after leaving the 2000 for carbs and proteins the remaining 400 calories can be used for fats . A doctor if regularly checks the sugar readings , knows the differences and danger signals. Accordingly changes can be made in the diet . I once again remind you that the monitoring is required in the initial stages , say about 6 months or so .later once in a month , after that once in 3 months , after that once in 6 months would do . An yearly check up of whole body gives the overall picture .This is only a suggestion and can be ignored if felt utter foolish concept . Herbs are not junk or trash and herbs like turmeric , gingkobiloba , sage , terminalia chebukaa , Ashwagandha , avenasathiva all help in maintaining the healthy state . Buts herbs have to selected depending upon the need . For example if worm problem is present azaridicta indica , general weakness ,frequent coughs and colds avena sathiva and ocimum , Frequent digestive disturbances sage like that . Arguments are over ,not because of no point in the content , but because of the attitude of the parties concerned .
Hidden
ππππ.
You are advising 250g carbs and 250g protein for this child πππ and saying his bs will be under control !! πππ. Too optimistic. And just 35 g oil !?? I don't agree at all. This is totally unscientific. Let's see how many people buy your idea here.
You want to give 3 major meals and 3 nibblings in between ! So you don't want beta cells to take rest ? You want to give laddu and fruits and chocolates. Here i'm saying that if you eat fruit you can't eat any carb then. And what bs levels are you expecting with your diet plan ?
Herbs and for that matter nothing will help as long as sugar is high.
"...because of the attitude of the parties concerned ." What about attitude ? Madam i want to learn from you.
But let's see who supports you.
β’ in reply tosuramo
Chacolates laddu , fruits all have to fit in to this allowed caloric consumption only . If this theory is not acceptable to the non believers , it is ok with me . No problem . But sugar would not be high when once the system gets used to this diet plan .
Hidden
"If this theory is not acceptable to the non believers , it is ok with me". This is not about believing you or me. We have to believe in science.
"But sugar would not be high when once the system gets used to this diet plan ." How ? He is type 1 so no chance of what you say. Even type 2 people become D when system gets upset.
1) how will you control bs with 250g carbs?
2)What is so inevitable about carb that you want to give it to t1 child and even t2d people ?
β’ in reply tosuramo
The meal plan is for child ,who is in the age group of 14 to 20 and very active with physical and mental activity and where growth spurt is high . The demands of caloriies could be less in children who are shorter and thinner . Now a days boys are reaching the height of 5feet 10 inches at the age of 15 years it self .Some 20 years back it was 5 feet only . Any way the caloric needs depend upon the height , weight , activity , etc . If the caloric need is 2400 units the carbs and proteins are 250 gms each . If it is 2000 or 1800 it would come down relatively . My point is lesser intake of protein is responsible for the incidence of diabetes in average Indian families . When the protein is reduced , naturally carb intake increases to satisfy the hunger pangs and to get the feeling of fullness which in its turn leads to more insulin need . The other alternative recently found is fats . But that too is ridden with risks . Only protein meal means kidney complications would arise . So a balance has to be set in where the child in growth stage should not depend more on insulin shots or modern medicines or should not be haunted by constant hunger pangs , should not feel deprived of ordinary happy childhood which is enjoyed by his peers . If not 250 gms of protein atleast 150 gms of protein can be given , I have been insisting on the wholesome food and not junk food and empty calories .Fruits , chacolates , goodies , yogurt all have to be calculated and included in this caloric restricted meal plan depending upon the ingredients which go in to the making of that particular food item fitting in the overall picture .
Hidden
"My point is lesser intake of protein is responsible for the incidence of diabetes in average Indian families . When the protein is reduced , naturally carb intake increases to satisfy the hunger pangs and to get the feeling of fullness which in its turn leads to more insulin need ". Where do you get this kind of information ? Indian diet is a balanced diet. Protein is provided in sufficient quantity. We need to modify carb intake in indian dish. The boy is type 1 so no q of taking high carb and turning insulin needs.
1) You still didn't answer how you will manage high bs levels with 250 odd g carbs ? You also recommend taking high protein. Both would need insulin.
2) What is inevitability of carbs ?
3) why are fats not desirable food ?
4) Fruits will cause nafld. Laddu contains sugar. Is sugar not junk or when added to grain ( which themselves are harmful ) it becomes nonjunk ?
β’ in reply to
the idea that beta cells need rest specially in this age group is a myth .In the growth period cells need more food and more activity . I don't go by half baked , funded research papers . The calculations given all are the most unreliable , whether it is cholesterol , sugar readings or any other parameters . FOR one real finding we have thousands of fake data Since we don't go by the fake reports , there is no need to depend on them .Who knows for all reported findings exactly opposite reports would be issued after 2 years .
Hidden
So are you saying that all the scientific research done on D by the world is fake - "half baked , funded research papers " πππ ?? So D people should not take sugar, high carb etc are all fake !? By the way we here don't talk on some funded research. We tell our own experience.
Anup, when is this seminar on LCHF? I am interested in attending it.
Thank you anup. But a pity I won't be in Bangalore as I'm off to Chennai tomorrow for a long weekend with my mother
suramoStar
Hidden ,
ππππ. Now arguments are exhausted so "please leave the issue here . ," ππ. There is an idea / logic first. Substantiated by scientific evidence. We don't need to "experiment " all the time. Lchf is now a proven fact. I don't know why Hidden is so adamant about high carb and /or high protein diet. But well leave the issue here.
swathy
"What is scientific It is not medicine . It is ordinary simple home cooked food ". Sorry madam. Our food is science and not ordinary simple home cooked food.
I'd still love to know what danger do you expect from 60% good fats?
suramoStar
Hidden ,
I know there is no danger. We don't have to look at the studies. We ourselves are taking high fat diet and doing quite well. Scientifically also there is no harm.
Half truths and statistics are not science .
The requirements of growth stage decide caloric consumption and the division of carbs and proteins depend on the total intake . It could be different depending upon the individual need of total calories..In case of 2400 calories the carbs or proteins are to be taken in 250 gms each .I told total carbs from all sources and total proteins from all sources .
What is this argument . I said 10 00 calories of carbs and 1000 calories of proteins and 400 calories of fats . and the total calories of 2400 for a child of 14 to 20 years Then 1000 calories come to 250 grams of carbs and 250 gms proteins .
I specifically said 1000 calories in carbs and 1000 calories in proteins which come to 250 gms of carbs and 250 gms of proteins and 400 calories in fats from all sources put together .PLEASE go to the op .
Each case has to work out the diet plan according to it's need with in the frame work of the calculated values . Any way let us wait for some time for getting the results . In the meanwhile let us hope the ranges of FBS , PPBS and hb1c do not come down further . CHOLESTEROL and BP ranges have changed already .
β’ in reply to
I would like to request moderators to give a thought to opening a separate unit for the alternative medicine , since diabetes has become a global epidemic and there is no reasonably reliable cure for the same in modern medicine . Who ever wants to try that cure can get all the information in that forum with out disturbing the present ideas and diets about diabetes .A fraction of people are always getting visibly agitated with the alternative methods and modes .
There is no point in defending my argument when there is so much of antagonism even to the suggestion . AFTER 5 to 6 years , wen many cases taking insulin shots or modern medicines and different diets spring up with dementias , parkinsons , alzheimers scizhophrenias , vitiligos or some strange mental maladies people would realise the after effects of the so called science .
An average 15 year old boy of 5 feet 4 inches height ,126 pounds of weight needs 350 gms carbs . 145 gms protein ,and 50 gms fats for the normal healthy growth and activity according to some .In case of type 1 since the carb content has to be reduced , 100 gms of carbs can be reduced from the carbs and some 30 gms can be reduced from fats and added to proteins to facilitate the production of glucagon .The composition can be worked out according to the dietary preferences fitting in to this plan . In this case experiment has to be done with regular monitoring . Since I do not have an idea about the protein content of various non veg items I can't give the meal plan with break up. Since it is case of D1 , case of the growth period , extra requirement of protein with new diet plan , all the extra caution is required . One or two stray cases do not set an example. Diabetes is a disorder which does not go by standard and uniform rules , if total and absolute cure is aimed at. Any way it is a suggestion only if any body wants to make a trial with extra precautions taken .
Yes/ Your views are well thought and based on experience in the field I have been a diabetic for more than 5 years. Now I am 66. In the initial stage, one doctor in Vizag prescribed me amaryl l mg. which controlled my sugar levels and even brought down below 100 Fasting. Then I came down to Chennai and here the Doctor reduced it to amaryl 0,5 mg. After some period, he changed the prescription to Glycomet 500 metformin tables twice a day and I have been continuing till date. Since the last 6 years I have started routing walkings for 30 minutes in the mornng and evening apart from 20 m normal exercise and occasional breathing exercise. Then my diet plan is changed as follows. 6 AM sugarless tea 8.30 am 3 or 4 medium sized idly or equivalent quantity of breakfast followed by glycomet 500. At 11.30AM 1 or 2 idly or equivalent quantity of other item then 1 cup of buttermilk or lemon juice with salt or plain tea whichever is available. Then at 2 pm meals with reduced rice say half of what i used to eat before 60 years of age - 3 or 4 handful size of table size spoon with plenty of vegetables and cucumber with sambar or rasam and buttermilk. No extra item like pickles, etc.,At 4.30 pm a light snack say a handful of grains or a light dosa with plain tea. Then at 8 pm dinner with only 2 chappatis or 2 millet dosas or equivalent quantity of other tiffin. No poori, potato, banana, other oily items. After dinner the glycomet tablet. That is all my diet plan daily for the past 6 years. Three or four days in a week, half of an apple or guava, or pomengrade or 5 pieces of papaya are taken. 2 almonds are taken during the last l years due to less HDL. Now the blood sugar is around 100 plus or minus 10 in Fasting and is around 180 FP during the last 3 years. I reduced my visit to doctor once in a quarter from monthly visit and also lab test once in a quarter., apart from the yearly master check up.. The final answer is that you have to live with the diabetes till your death but manage/control it with a fixed diet plan sacrificing sweets and oils and with a change in life style and regular moderate exercises. Long walkings of more than 6 to 8 kms. daily may result in bone pain in the old age of around 80 years as happened to some of my friends and relatives. Be moderate in everything you do for a healthy and peaceful life. God will bless you all in this forum.
I need to know his age, weight, height, other diseases (if any), profession andnature of physical work he does in a day to make any comment on him. But if it's type-1 then he has to take insulin on daily basis as his pancreaus does not produce insulin at all or a little amount. His daily physical activity will determine his diet i.e. protein:carb:fat.
Hey guys, why cannot we answer the question asked first, then suggest other solutions after. The person wanted more information on Insulin implants! It's been a nightmare to get direct responses on this questionβΉ ?
Activity2004Administrator
Hidden ,
What about Low Carb High Protein? Does that work for a type 1 diabetic?
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