Budwig Diet- Meals that are anti-cancer, anti-diabetic...

[sense]

Who are you exactly?

 

[Jah_rastafar_I]

Sense if you really want to help you would have e-mailed dr sam already and offered to help him publish his works instead of posting in this forum talking nonsense and asking any of us to pte msg you on publishing sam's works. None of us know sam personally how could we send you his stuff?

 

[Fook Seng]

It's alright to be suspicious. If someone made all these claims I would want more facts before paying $$$ for the treatment.

I am just a fellow forummer looking for answers & not a self proclaim expert. But if true, this is ground breaking stuff & it would solve many of my medical problems It would also threaten the livehoods of many doctors

If you are intent on solving your diabetes problem, there is a study, I believe, from UK that if you go on a 600 calories diet for 2 months and thereafter do reasonable diet, your Type 2 diabetes will be gone for good. Of course during the dieting, you should stop all your medication and your alternative diet. A 600 calorie a day is a very extreme diet, like taking juice only. It has to properly supervise by a medical practitioner. I doubt a normal GP will do it for you. As for cancer, heart problem or type 1 diabetes, there seems to be some vaccines being developed, need clinical testing of course. You can find details of this in the October 2011 issue of the Discover magazine (31st Anniversary Special Issue). Should still be available in the bookshops. Cover has the words "cure everything" in large letters.

 

[johnny333]

How did you find Sam Chachoua's explaination of how cancers are formed and also the hayflick limit in which the cell has a limited number of times to replicate before it's unable to do so typically the number would be 50 times. The cell turns cancerous cos cancer cells are the only cells not bound by the hayflick limit.

In the vid he explains how the ppl with cancer don't seem to be infected with any infectious diseases and how ppl with cancers seem to be a perfect mirror image of those with infectious diseases. At places where ppl had infectious diseases, ppl with cancers were so few and it was the opposite when ppl had cancers.

Causes of cancers are so vast and varied and unknown. Ppl that don't smoke can also develop lung cancer and when asked for the reason why drs will give some vague answer like maybe it was due to stress maybe it was a pink flying elephant, this and that.

It then gives cause to reason that cancer is the body's own natural way to protect against infectious diseases or to go against the hayflick limit. I didn't watch the video in its entirety so i don't know if he explained how developing cancerous cells would actually help someone whose cells in some organ perhaps the lungs had reached the hayflick limit and having cancerous cells would help.

I've come across the hayflick theory in articles about human longevity. They theorise that as we age, we reach our hayflick limit & the cells start to make faulty copies.
It may also explain why some people who smoke don't get cancer.

I've often wondered why I developed heart problems at an early age. I suspect it was from trauma that I experienced years ago when I broke both legs & exposure to numerous xrays I had from that experience. In those days word like trauma & inflamation was commonly used instead of hayflicks. I guess I've reached my upper hayflick limit.:(

 

[sense]

If you are intent on solving your diabetes problem, there is a study, I believe, from UK that if you go on a 600 calories diet for 2 months and thereafter do reasonable diet...

Scott Baker, George Jerums, Joseph Proietto, Effects and clinical potential of very-low-calorie diets (VLCDs) in type 2 diabetes, Diabetes Research and Clinical Practice, Volume 85, Issue 3, September 2009, Pages 235-242, ISSN 0168-8227, 10.1016/j.diabres.2009.06.002.
(http://www.sciencedirect.com/science/article/pii/S0168822709002502)
Abstract: A recent study has shown that obese patients with newly diagnosed type 2 diabetes who lose 10% of their body weight are more likely to achieve glycaemic and blood pressure targets, despite weight regain. A well-established non-surgical method for achieving weight loss ≥10% within 3 months is the use of very-low-calorie diets (VLCDs). In patients with diabetes, VLCDs are associated with rapid improvement in glycaemia and cardiovascular risk factors. The present review analyses the evidence from available trials on the effects of VLCDs on body weight, glycaemic control and complications, and their potential for clinical use in diabetes management.
Keywords: Very-low-calorie diets; Type 2 diabetes; Weight loss

Marieke Snel, Maria A. Sleddering, Inge D. vd Peijl, Johannes A. Romijn, Hanno Pijl, A. Edo Meinders, Ingrid M. Jazet, Quality of life in type 2 diabetes mellitus after a very low calorie diet and exercise, European Journal of Internal Medicine, Available online 17 August 2011, ISSN 0953-6205, 10.1016/j.ejim.2011.07.004.
(http://www.sciencedirect.com/science/article/pii/S095362051100149X)
Abstract: Objective
To evaluate whether the addition of exercise to a very low calorie diet (VLCD) has beneficial short- and long-term effects on health-related quality of life (QoL) in obese patients with type 2 diabetes mellitus (T2DM).
Methods
We included 27 obese, insulin-dependent T2DM patients in a 16-week VLCD study, of whom 13 participated simultaneously in an exercise program (VLCD + E). Before, immediately after and 18 months after the intervention anthropometric measurements, glucoregulation and QoL (SF-36, HADS, NHP and MFI-20) were assessed. Patients were compared to healthy lean and obese (matched for body mass index) controls matched for gender and age.
Results
At baseline, T2DM patients had significantly worse QoL scores in 18 and 14 of the 22 subscales of the QoL questionnaires, compared to lean and obese controls, resp. The 16-week VLCD (n = 27) decreased bodyweight (− 25.4 ± 1.3 kg, p < 0.0001, p = 0.179 between groups), and improved glucoregulation (HbA1c − 1.3 ± 0.3%, p < 0.0001, p = 0.488 between groups) and 9 (VLCD-only) and 11 (VLCD + E) of the 22 subscales of QoL.

After 18 months, in the VLCD + E group the QoL subscales did not differ from those in obese controls and only 4 of the 22 subscales were significantly worse compared to lean controls. However, in the VLCD-only group 17 and 13 of the 22 QoL subscales were significantly worse compared to the lean and obese controls, resp.
Conclusion
A 16-week VLCD induces considerable weight loss, metabolic amelioration, and major improvements in QoL in obese T2DM patients. The addition of exercise is of paramount importance for the maintenance of better QoL.
Keywords: Type 2 diabetes mellitus; Quality of life; Very low calorie diet; Exercise; Glycemic control

Masahiro Fukuda, Yasuhiro Tahara, Yoshihiro Yamamoto, Toshio Onishi, Yuichi Kumahara, Akira Tanaka, Kenji Shima, Effects of very-low-calorie diet weight reduction on glucose tolerance, insulin secretion, and insulin resistance in obese non-insulin-dependent diabetics, Diabetes Research and Clinical Practice, Volume 7, Issue 1, 1989, Pages 61-67, ISSN 0168-8227, 10.1016/0168-8227(89)90047-8.
(http://www.sciencedirect.com/science/article/pii/0168822789900478)
Abstract: We put 12 obese subjects on a very-low-calorie diet (VLCD) and observed how their weight loss affected their glucose tolerance. Seven had non-insulin-dependent diabetes and five did not. They consumed 1000 kcal/day for at least 1 week, then 420 kcal/day for 4 weeks, and 1000 kcal/day thereafter. VLCD improved glucose tolerance and insulin response to a glucose load in the diabetics and did not affect these parameters in the non-diabetics. It did not change insulin responsiveness to intravenous glucagon in either group. Both groups showed improved insulin resistance, as measured by an insulin suppression test. Regression analysis showed that insulin resistance correlates well with obesity and glycemic control. Weight reduction did not change hepatic insulin extraction. Thus, the improvement in glucose tolerance by some of the diabetics seems to have arisen from improvements in their insulin resistance and insulin response to a glucose load. Insulin resistance improved because of weight reduction and subsequent improvements in glycemic control.
Keywords: Obesity; Very-low-calorie diet; Insulin resistance; Insulin responsiveness

Marieke Snel, Janna A. v Diepen, T. Stijnen, Hanno Pijl, Johannes A. Romijn, A. Edo Meinders, Peter Voshol, Ingrid M. Jazet, Immediate and Long-term Effects of addition of exercise to a 16-week Very Low Calorie Diet on Low-grade Inflammation in Obese, Insulin-dependent Type 2 Diabetic Patients, Food and Chemical Toxicology, Available online 4 October 2011, ISSN 0278-6915, 10.1016/j.fct.2011.09.032.
(http://www.sciencedirect.com/science/article/pii/S0278691511004844)
Abstract: Objective
To assess the short- and long-term effects of addition of exercise to a very low calorie diet (VLCD) on low-grade inflammation in obese patients with type 2 diabetes mellitus (T2DM).
Methods
27 obese, insulin-dependent T2DM patients followed a 4-month VLCD with (n=13) or without (n=14) exercise and were followed up to 18 months. Anthropometric measurements, metabolic and inflammatory parameters were assessed before, directly after the intervention and at 6 and 18 months follow-up. The same measurements were performed only once in 56 healthy lean and 56 healthy obese controls.
Results
At baseline hsCRP, IL10 and IL8 were significantly elevated in obese T2DM compared to lean healthy controls. After 4 months, despite substantial weight loss (-25.4±1.3kg), neither the VLCD nor VLCD + exercise had an effect on plasma cytokines. At 6 months, in the weight-stabilizing period, measures of low-grade inflammation had decreased substantially and equally in both intervention groups. Despite subsequent weight regain, beneficial effect was sustained up to 18 months in both groups, except for IL1 and hsCRP which had returned to baseline in the VLCD-only group.
Conclusion
Our findings suggest that severe caloric restriction increases cytokine production by adipose tissue macrophages and that the beneficial effects of weight loss become apparent only in the eucaloric state.
Keywords: cytokines; hsCRP; adipose tissue; weight loss; calorie restriction

 

[johnny333]

If you are intent on solving your diabetes problem, there is a study, I believe, from UK that if you go on a 600 calories diet for 2 months and thereafter do reasonable diet, your Type 2 diabetes will be gone for good. Of course during the dieting, you should stop all your medication and your alternative diet. A 600 calorie a day is a very extreme diet, like taking juice only. It has to properly supervise by a medical practitioner. I doubt a normal GP will do it for you. As for cancer, heart problem or type 1 diabetes, there seems to be some vaccines being developed, need clinical testing of course. You can find details of this in the October 2011 issue of the Discover magazine (31st Anniversary Special Issue). Should still be available in the bookshops. Cover has the words "cure everything" in large letters.

I've read of some cures for type II but the problem is that it takes about 60 days. This is the time it takes for the body to replace it's cells & even if you cure syndrome X(Type II) you have to avoid all transfats, hydrogenationed fats, etc or face the same problem again.

If anyone has any doubts about the dangers of transfats, all you have to do is look at the US where there i is an epidemic of teens getting diabetes.

 

[sense]

I've come across the hayflick theory in articles about human longevity. They theorise that as we age, we reach our hayflick limit & the cells start to make faulty copies...

A. Golubev, S. Khrustalev, A. Butov, An in silico investigation into the causes of telomere length heterogeneity and its implications for the Hayflick limit, Journal of Theoretical Biology, Volume 225, Issue 2, 21 November 2003, Pages 153-170, ISSN 0022-5193, 10.1016/S0022-5193(03)00229-7.
(http://www.sciencedirect.com/science/article/pii/S0022519303002297)
Abstract: In telomerase-negative cell populations the mean telomere length (TL) decreases with increasing population doubling number (PD). A critically small TL is believed to stop cell proliferation at a cell-, age- and species-specific PD thus defining the Hayflick limit. However, positively skewed TL distributions are broad compared to differences between initial and final mean TL and strongly overlap at middle and late PD, which is inconsistent with a limiting role of TL. We used computer-assisted modelling to define what set of premises may account for the above. Our model incorporates the following concepts. DNA end replication problem: telomeres loose 1 shortening unit (SU) upon each cell division. Free radical-caused TL decrease: telomeres experience random events resulting in the loss of a random SU number within a remaining TL. Stochasticity of gene expression and cell differentiation: cells experience random events inducing mitoses or committing cells to proliferation arrest, the latter option requiring a specified number of mitoses to be passed. Cells whose TL reaches 1 SU cannot divide. The proliferation kinetics of such virtual cells conforms to the transition probability model of cell cycle. When no committing events occur and at realistic SU estimates of the initial TL, maximal PD values far exceed the Hayflick limit observed in normal cells and are consistent with the crisis stage entered by transformed cells that have surpassed the Hayflick limit. At intermediate PD, symmetrical TL distributions are yielded. Upon introduction of committing events making the ratio of the rates of proliferating and committing events (P/C) range from 1.10 to 1.25, TL distributions at intermediate PD become positively skewed, and virtual cell clones show bimodal size distributions. At P/C as high as 1.25 the majority of virtual cells at maximal PD contain telomeres with TL&gt;1 SU. A 10% increase in P/C within the 1.10–1.25 range produces a two-fold increase in the maximal PD, which can reach values of up to 25 observed in rodent and some human cells. Increasing the number of committed mitoses from 0 to 10 can increases PD to about 50 observed in human fibroblasts. Introduction of the random TL breakage makes the shapes of TL distributions quite dissimilar from those observed in real cells. Conclusions: Telomere length decrease is a correlate of cell proliferation that cannot alone account for the Hayflick limit, which primarily depends on parameters of cell population kinetics. Free radical damage influences the Hayflick limit not through TL but rather by affecting the ratio of the rates of events that commit cells to mitoses or to proliferation arrest.
Keywords: Telomere; Hayflick's limit; Cell cycle; Cell aging; Model; Stochastic processes

David A. Juckett, Cellular aging (The hayflick limit) and species longevity: A unification model based on clonal succession, Mechanisms of Ageing and Development, Volume 38, Issue 1, March 1987, Pages 49-71, ISSN 0047-6374, 10.1016/0047-6374(87)90110-2.
(http://www.sciencedirect.com/science/article/pii/0047637487901102)
Abstract: A model is presented which proposes a specific cause-and-effect relationship between a limited cell division potential and the maximum lifespan of humans and other mammals. It is based on the clonal succession hypothesis of Kay [1] which states that continually replicating cell beds (e.g. bone marrow, intestinal crypts, epidermis) could be composed of cells with short, well-defined division potentials. In this model, the cells of these beds are proposed to exist in an ordered hierarchy which establishes a specific sequence for cell divisions throughout the organism's lifespan. The depletion of division potential at all hierarchical levels leads to a loss of bed function and sets an intrinsic limit to species longevity. A specific hierarchy for cell proliferation is defined which allows the calculation of time to bed depletion and, ultimately, to organism mortality. The model allows the existence of a small number (n) of critical cell beds within the organism and defines organism death as the inability of any one of these beds to produce cells. The model is consistent with all major observations related to cellular and organismic aging. In particular, it links the PDLs (population doubling limit) observed for various species to their mean lifespan; it explains the slow decline in PDL as a function of age of the donor; it establishes a thermodynamically stable maximum lifespan for a disease-free population; and it can explain why tissue transplants outlive donors or hosts.
Keywords: Aging; Stem cells; Clonal succession; Hayflick limit; Lifespan; Mathematical model

Rita B. Effros, Replicative Senescence in the Immune System: Impact of the Hayflick Limit on T-Cell Function in the Elderly, The American Journal of Human Genetics, Volume 62, Issue 5, May 1998, Pages 1003-1007, ISSN 0002-9297, 10.1086/301845.
(http://www.sciencedirect.com/science/article/pii/S0002929707615183)
Keywords: Senescence; Immune system; Hayflick limit; T cells; Aging; Replicative senescence

Hans J. Bremermann, Reliability of proliferation controls. The Hayflick limit and its breakdown in cancer, Journal of Theoretical Biology, Volume 97, Issue 4, 21 August 1982, Pages 641-662, ISSN 0022-5193, 10.1016/0022-5193(82)90364-2.
(http://www.sciencedirect.com/science/article/pii/0022519382903642)
Abstract: This paper presents a new theory of the Hayflick limit and its role in cancer. The Hayflick limit is identified as a fail-safe mechanism that limits to harmless size descendent clones of cells in which normal proliferation controls have broken down. Malignancy arises when the Hayflick limit is inactivated. It is argued that the Hayflick limit is due to differentiation towards a non-proliferating state. Redundant developmental clocks are envisioned as the mechanism. Chemical carcinogens and promoters can interfere with these clocks. Also, viral gene products and integration of viral DNA can stop the developmental clock and lead to malignant transformation in cells that have already suffered mutations in their normal regulatory mechanisms that control proliferation. Viral transformation can be understood as a viral strategy of survival and transmission to a new host. Malignant clones may constitute a niche for many slow viruses. Normal functioning of the Hayflick limit implies senescence of tissues due to differentiation towards a non-proliferating state. Hence, the limit may be the cause of senescence even though it is not due to an accumulation of somatic mutations.

Rita B. Effros, Roy L. Walford, T cell cultures and the Hayflick limit, Human Immunology, Volume 9, Issue 1, January 1984, Pages 49-65, ISSN 0198-8859, 10.1016/0198-8859(84)90006-5.
(http://www.sciencedirect.com/science/article/pii/0198885984900065)

P. Naveilhan, C. Baudet, W. Jabbour, D. Wion, A theory that may explain the Hayflick limit — a means to delete one copy of a repeating sequence during each cell cycle in certain human cells such as fibroblasts, Mechanisms of Ageing and Development, Volume 75, Issue 3, September 1994, Pages 205-213, ISSN 0047-6374, 10.1016/0047-6374(94)90010-8.
(http://www.sciencedirect.com/science/article/pii/0047637494900108)
Abstract: A model that may explain the limited division potential of certain cells such as human fibroblasts in culture is presented. The central postulate of this theory is that there exists, prior to certain key exons that code for materials needed for cell division, a unique sequence of specific repeating segments of DNA. One copy of such repeating segments is deleted during each cell cycle in cells that are not protected from such deletion through methylation of their cytosine residues. According to this theory, the means through which such repeated sequences are removed, one per cycle, is through the sequential action of enzymes that act much as bacterial restriction enzymes do — namely to produce scissions in both strands of DNA in areas that correspond to the DNA base sequence recognition specificities of such enzymes. After the first scission early in a replicative cycle, that enzyme becomes inhibited, but the cleavage of the first site exposes the closest site in the repetitive element to the action of a second restriction enzyme after which that enzyme also becomes inhibited. Then repair occurs, regenerating the original first site. Through this sequential activation and inhibition of two different restriction enzymes, only one copy of the repeating sequence is deleted during each cell cycle. In effect, the repeating sequence operates as a precise counter of the numbers of cell doubling that have occured since the cells involved differentiated during development.
Keywords: Replicative senescence; Restriction enzyme; Aging; Mitosis

Geoff Watts, Leonard Hayflick and the limits of ageing, The Lancet, Volume 377, Issue 9783, 18-24 June 2011, Page 2075, ISSN 0140-6736, 10.1016/S0140-6736(11)60908-2.
(http://www.sciencedirect.com/science/article/pii/S0140673611609082)

Rita B. Effros, Graham Pawelec, Replicative senescence of T cells: does the Hayflick Limit lead to immune exhaustion?, Immunology Today, Volume 18, Issue 9, September 1997, Pages 450-454, ISSN 0167-5699, 10.1016/S0167-5699(97)01079-7.
(http://www.sciencedirect.com/science/article/pii/S0167569997010797)
Abstract: Extensive in vitro research on fibroblasts has defined numerous genetic and phenotypic changes associated with replicative senescence. Identification of T-cell replicative senescence as a feature of human immunodeficiency virus (HIV) disease and ageing suggests this phenomenon merits more careful consideration by immunologists, especially with regard to chronic infection, memory and adoptive immunotherapy.

Rita B. Effros, Impact of the Hayflick Limit on T cell responses to infection: lessons from aging and HIV disease, Mechanisms of Ageing and Development, Volume 125, Issue 2, February 2004, Pages 103-106, ISSN 0047-6374, 10.1016/j.mad.2003.11.003.
(http://www.sciencedirect.com/science/article/pii/S0047637403002227)
Abstract: Aging and HIV disease show certain immunological similarities. In both situations, control over viral infection is diminished, and there is an increase in certain types of cancer. The immune cell type responsible for controlling viral infections and cancer is the so-called CD8 or cytotoxic T cell. In elderly persons and individuals chronically infected with HIV, there are high proportions of CD8 T cells that resemble cells that reach the end stage of replicative senescence in cell culture after repeated rounds of antigen-driven proliferation. Senescent cultures are characterized by irreversible cell cycle arrest, shortened telomeres, inability to upregulate telomerase, loss of CD28 expression, and apoptosis resistance. Strategies that retard replicative senescence may, therefore, provide novel approaches to enhancing immune function during aging and HIV disease.
Keywords: T cells; Replicative senescence; Aging; HIV disease

Olivier Toussaint, Jose Remacle, Jean-François Dierick, Thierry Pascal, Christophe Frippiat, Stéphanie Zdanov, Joao Pedro Magalhaes, Véronique Royer, Florence Chainiaux, From the Hayflick mosaic to the mosaics of ageing.: Role of stress-induced premature senescence in human ageing, The International Journal of Biochemistry &amp; Cell Biology, Volume 34, Issue 11, November 2002, Pages 1415-1429, ISSN 1357-2725, 10.1016/S1357-2725(02)00034-1.
(http://www.sciencedirect.com/science/article/pii/S1357272502000341)
Abstract: The Hayflick limit—senescence of proliferative cell types—is a fundamental feature of proliferative cells in vitro. Various human proliferative cell types exposed in vitro to many types of subcytotoxic stresses undergo stress-induced premature senescence (SIPS) (also called stress-induced premature senescence-like phenotype, according to the definition of senescence). The known mechanisms of appearance the main features of SIPS are reviewed: senescent-like morphology, growth arrest, senescence-related changes in gene expression, telomere shortening. Long before telomere-shortening induces senescence, other factors such as culture conditions or lack of ‘feeder cells’ can trigger either SIPS or prolonged reversible G0 phase of the cell cycle. In vivo, ‘proliferative’ cell types of aged individuals are likely to compose a mosaic made of cells irreversibly growth arrested or not. The higher level of stress to which these cells have been exposed throughout their life span, the higher proportion of the cells of this mosaic will be in SIPS rather than in telomere-shortening dependent senescence. All cell types undergoing SIPS in vivo, most notably the ones in stressful conditions, are likely to participate in the tissular changes observed along ageing. For instance, human diploid fibroblasts (HDFs) exposed in vivo and in vitro to pro-inflammatory cytokines display biomarkers of senescence and might participate in the degradation of the extracellular matrix observed in ageing.
Keywords: Senescence; Oxidative stress; Telomeres; Apolipoprotein J; TGF-β1; Ageing

 

[johnny333]

This thread is about a diet that will help prevent cancer and diabetes. Let's leave diabetes out of this and focus solely on cancer. This diet has its naysayers as proven by screwballs rants. That's normal. There's probably hundreds of diets out there that claim the same thing. Maybe they work maybe they don't. Maybe this diet works for some ppl but probably won't work for others.

What's exciting about Sams treatment is that it's not limited to just cancer & heart problems. To fully appreciate this treatment one has to view the video, at least the 2nd half.

 

[Unrepented]

After the heart attack, my bro kenna liver hep A, as well as kidney problem :(

Recently, he kenna diabetes also. Currently, my bro need to take two pills to help convert sugar to carbo. I really hope he can reduce his medication for the sake of his liver. Any opinion to reduce his sugar level?

What's exciting about Sams treatment is that it's not limited to just cancer & heart problems. To fully appreciate this treatment one has to view the video, at least the 2nd half.

 

[Fook Seng]

After the heart attack, my kenna liver hep A, as well as kidney problem :(

Recently, he kenna diabetes also. Currently, my bro need to take two pills to help convert sugar to carbo. I really hope he can reduce his medication for the sake of his liver. Any opinion to reduce his sugar level?

Eat less sugar (no soft drinks) and less rice and other carbohydrates like noodles as they can be converted to sugar. Lots of exercise.

 

[Unrepented]

Thanks.

My bro did exercise as much as his current condition allows, sweated and alleviated his water retention condition. Just wanted some opinion from forumers on what more can he do to improve his condition inorder to reduce his dependence on medication.

Since less rice and noodles, will brown rice help? Given the traditional asian diet, what can he take to replace rice and noodles?

Eat less sugar (no soft drinks) and less rice and other carbohydrates like noodles as they can be converted to sugar. Lots of exercise.

 

[johnny333]

Thanks.

My bro did exercise as much as his current condition allows, sweated and alleviated his water retention condition. Just wanted some opinion from forumers on what more can he do to improve his condition inorder to reduce his dependence on medication.

Since less rice and noodles, will brown rice help? Given the traditional asian diet, what can he take to replace rice and noodles?

Your brothers case sounds very serious. Having illnesses on top of diabetes can complicate matters. When I had the flu recently, I developed water retention problems. Had to go see a doctor who injected me with insulin & then set me up with an IV drip. After I received 3 bottles, I had to go to the loo very often for the next couple of days.

Is your brother under a doctors care

 

[Fook Seng]

Thanks.

My bro did exercise as much as his current condition allows, sweated and alleviated his water retention condition. Just wanted some opinion from forumers on what more can he do to improve his condition inorder to reduce his dependence on medication.

Since less rice and noodles, will brown rice help? Given the traditional asian diet, what can he take to replace rice and noodles?

Brown rice has more fibre and some vitamins but essentially it is still carbohydrate. Basically the quantity should be reduced, say to two-thirds of a bowl. Replace energy requirement with tofu and proteins such as fish. Although protein is also a source of energy, too much of it will stress some other organ. The dietician will recommend a balanced diet with less carbo but more vegetables, tofu and fish for protein.

 

[Unrepented]

No. not under doctor's care, just need to go back for routine checkups.

All the problems started after the heart attack:(

Your brothers case sounds very serious. Having illnesses on top of diabetes can complicate matters. When I had the flu recently, I developed water retention problems. Had to go see a doctor who injected me with insulin & then set me up with an IV drip. After I received 3 bottles, I had to go to the loo very often for the next couple of days.

Is your brother under a doctors care

 

[Unrepented]

I think I should check with him if the hospital assigned him any resident dietician to advice him on dieting. Thanks for the reminder.

Brown rice has more fibre and some vitamins but essentially it is still carbohydrate. Basically the quantity should be reduced, say to two-thirds of a bowl. Replace energy requirement with tofu and proteins such as fish. Although protein is also a source of energy, too much of it will stress some other organ. The dietician will recommend a balanced diet with less carbo but more vegetables, tofu and fish for protein.

 

[Unrepented]

You can trying breathing exercises in the morning and maybe takeup cycling around any park in the afternoon to sweat it out or do rowing machine to reduce the water retention.

Your brothers case sounds very serious. Having illnesses on top of diabetes can complicate matters. When I had the flu recently, I developed water retention problems. Had to go see a doctor who injected me with insulin & then set me up with an IV drip. After I received 3 bottles, I had to go to the loo very often for the next couple of days.

Is your brother under a doctors care

 

[Fook Seng]

I think I should check with him if the hospital assigned him any resident dietician to advice him on dieting. Thanks for the reminder.

This specialist at SGH is quite good. His name is Dr Lim Heok Seng. He believes in dieting and will recommend a dietician from the hospital to provide advice. Recently we was bestowed the title of Dato by the Brunei Sultan. Don't worry. His fees are normal.

 

[johnny333]

No. not under doctor's care, just need to go back for routine checkups.

All the problems started after the heart attack:(

What's more important is that he develop a relation with a doctor he trusts. So that in future you can go back to same doctor for advise or if things take a turn for the worse.
I go to a doctor in JB & if I need to I can get medical help 7 days a week. Although he is just an MD, he has experience with patients suffering from heart & diabetes problems.

As a diabetic your brother should learn about the low glycemic foods. This means avoiding potatoes, refined starches, processed foods, transfats, hydrogenated oils(margarine), sugars. He should never eat at any fast food chains. He should avoid ALL processed foods

He must start eating at home where he can control what goes into the foods he eats. The reason I recommend the Budwig protocol is that it is easy & fast to prepare & is nutritious. The other healthy foods require more time to prepare as they require heating, steaming, etc. The recommended diet for people with his problem is fresh steamed vegetables, fibre, legumes, etc Avoid saturated fats.

He should start to read food labels & avoid 95% of the foods sold at NTUC

Learn about the herbs/spices/supplements that help his condition e.g. salmon(fish oil), onions(garlic), cinnamon, bitter gourd, gymnema. Take at least a mult-vitamin & some of these to help control the sugars.

My doctor prescribed metformin(glucophage) for me. I sometimes take it but when it comes to medication he has to consult with a doctor. If he needs metformin he can get it at JB cheaper than in Spore

Making drastic lifestyle changes is necessary until his condition stabilises .

 

[johnny333]

You can trying breathing exercises in the morning and maybe takeup cycling around any park in the afternoon to sweat it out or do rowing machine to reduce the water retention.

Walking up & down stairs is as effective. I walk to the mall & around the mall for exercise.

When I had water retention problems it was painful to put on shoes because my legs & feet was swollen. Water started building up in my lungs & I coughed alot. I had to take diuretics like frusemide & spironolacyone to clear the liquid. Fortunately I'm now ok & don't have to take any medication.

 

[tonychat]

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