Hà Nội: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb...

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Hình minh hoạ là 1 bài báo cáo khoa học đăng trên trang web của Hiệp hội Sản Phụ Khoa Hoa Kì (American Congress of Obstetricians and Gynecologists ), có đề cập tới ứng dụng và các nghiên cứu về việc áp dụng chế độ low carb để điều trị vô sinh.

Vì hiện nay khoa học đã chứng minh nhiều trường hợp vô sinh gây ra do rối loạn chuyển hoá và có liên quan trực tiếp tới hội chứng rối loạn chuyển hoá insulin ( hệ quả của việc ăn quá nhiều Carb).

Ví dụ như bệnh buồng trứng đa nang ( polycystic ovarian syndrome) là 1 hệ quả của chứng rối loạn chuyển hoá gây vô sinh ở các chị em.

Chuối truớc đây cũng có nghiên cứu nhiều về vấn đề này. Nhưng ít khi đưa ra trên Facebook vì nghĩ vấn đề này nó hơi "nhạy cảm" với cả ít người quan tâm. Hơn nữa, mình là đàn ông đi nói với mọi người mình nghiên cứu cái này thấy nó kì kì sao đó )

Nhưng dạo gần đây thấy có 1 số Dì có vẻ quan tâm tới chủ đề này. Nếu như các Dì thực sự quan tâm và muốn tìm hiểu về chủ đề này thì các Dì bấm like và comment vào bài này nhé. Để Chuối biết các Dì thực sự quan tâm, và sẽ tiến hành post các bài viết về chủ đề này.

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

High Protein, Low Carb Diets Greatly Improve Fertility

May 6, 2013

New Orleans, LA -- A diet rich in proteins appears to have a pronounced positive effect on fertility, according to new research presented today at the Annual Clinical Meeting of The American College of Obstetricians and Gynecologists. Women undergoing in vitro fertilization (IVF) treatments who consumed high levels of protein and low levels of carbohydrates had better quality eggs and embryos.

Research led by Jeffrey B. Russell, MD, at the Delaware Institute for Reproductive Medicine (DIRM) in Newark, showed that patients whose daily protein intake was 25% or more of their diet and whose carbohydrate intake was 40% or less of their diet had four times the pregnancy rates of patients who ate less protein and more carbs daily before and during IVF cycles.

“Protein is essential for good quality embryos and better egg quality, it turns out,” said Dr. Russell. Between January 2010 and December 2011, 120 patients participating in an assisted-reproduction therapy program at DIRM completed a three-day nutritional log and had an embryo transfer. The diet diaries revealed that 48 patients had an average daily protein intake greater than 25% vs. 72% who had less than 25%. No differences were found in body mass index (BMI) in either group.

Embryo development was assessed after five days of culture or at the blastocyst stage. An increased blastocyst formation was found in 54.3% of patients whose daily protein intake was greater than 25% vs. 38% blastocyst formation in patients whose daily protein intake was less than 25%. The pregnancy rate was also significantly improved in patients with greater than 25% daily protein intake (66.6 % vs. 31.9%).

Dr. Russell pointed out that although BMI is implicated in reduced fertility, he had been seeing poor quality embryos among thin and healthy women. This made him want to take a closer look. After patients filled out their nutritional logs, Dr. Russell was surprised to see a large percentage of the women eating more than 60% carbs each day and 10% (or less) protein. These diets were associated with poor quality embryos.

Dr. Russell now requires patients to eat 25% to 35% protein and 40% or less carbs for three months before allowing them to begin their IVF cycles. His colleagues have also begun doing the same, he said.


YouTube Hear more with Dr. Russell.

*Monday Poster #96: Daily Protein Content Correlates with Increased Fertility and Pregnancy Outcome

The American College of Obstetricians and Gynecologists (The College), a 501(c)(3) organization, is the nation’s leading group of physicians providing health care for women. As a private, voluntary, nonprofit membership organization of more than 57,000 members, The College strongly advocates for quality health care for women, maintains the highest standards of clinical practice and continuing education of its members, promotes patient education, and increases awareness among its members and the public of the changing issues facing women’s health care. The American Congress of Obstetricians and Gynecologists (ACOG), a 501(c)(6) organization, is its companion organization. www.acog.org

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Đây là mess của 1 bác sỹ công tác tại bệnh viện nội tiêt. Vì mess dài nên Chuối cắt ra và ghép lại để các Dì đọc cho dễ dàng.

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Tế bào ung thư ko đơn giản chỉ sống bằng Glucose mà so với tế bào bình thường, thì nó có khả năng hấp thụ Glucose gấp 20 lần. Tức lượng đường Glucose chúng ta ăn vào người bao nhiêu thì tế bào ung thư ngay lập tức hút lấy và ăn 1 cách mãnh liệt để sinh tồn và phát triển.

Điều này xảy ra đó là do tế bào ung thư đã bị biến đổi thành phần cấu trúc gen cho nên có cơ chế hấp thụ năng lượng và hoạt động khác hẳn tế bào bình thường.

Đây là 1 trong những phát hiện quan trọng bậc nhất của ngành ung thư do Otto Warburg nhà sinh lý người Đức được 2 lần trao giải Nobel.

Phát hiện này của Warburg tuy ko được ứng dụng vào đại trà để chữa bênh ung thư ( vì nó ko đem lại tiền). Nhưng dựa theo phát hiện này người ta đã phát minh ra máy chụp PET (Positron emission tomography) để chuẩn đoán sớm khối u bị ung thư.

Nguyên lí hoạt động của máy chụp PET có thể giải thích đơn giản là xác định xem bộ phân nào của cơ thể có xảy ra sự hấp thụ Glucose 1 cách bất thường và mãnh liệt --> khu vực đó bị ung thư.

Ví dụ như hình minh hoạ là hình chụp PET của 1 người đàn ông bị ung thư não. Ở bên phải là cột chỉ định mức hấp thụ Glucose.

Chúng ta có thể thấy phần màu vàng bên trái ở dưới là khu vực tế bào ung thư đang hấp thụ đường Glucose rất mạnh nên có màu sắc khác hẳn so với khu vực màu xanh xung quanh của não. Và như thế khu vực đó đang bị ung thư.

Có một điều kì lạ, đó là trong ngành Y Tế từ lâu họ đã biết cách dựa theo mức độ hấp thụ Glucose của tế bào trong cơ thể để chẩn đoán ung thư. Tức họ biết ung thư sống bằng Glucose và hấp thụ rất mãnh liệt.

Nhưng ko có bác sỹ nào khuyên bệnh nhân phải kiêng Carb cả ( Carb sản sinh ra Glucose ).

Như thế ko khác gì đi xét nghiệm ma tuý, bác sỹ dựa theo hàm lượng ma tuý có trong nước tiểu, có trong máu của người nghiện. Nhưng bác sỹ vẫn cứ khuyên người nghiện ma tuý tiếp tục hút rồi để bác sỹ bán thuốc chữa nghiện ????

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Cancer Cell Metabolism

The internet is a wonderful thing, information really becomes available at our fingertips. Like everything, with the good comes the bad and, when we speak of cancer, a lot of bad information is unfortunately published. Everybody seems to have his/her own interpretation of the Warburg theory. In this document I'll try to clarify what this theory is and what we know about cancer cell metabolism.

The Warburg Effect

In 1931 Otto Heinrich Warburg was attributed the Nobel price in Physiology and Medicine mainly for his investigation of the metabolism of tumours and the respiration of cells, and more particularly for his discovery of the nature and mode of action of respiratory enzymes. He edited and has much of his original work published in The Metabolism of Tumours (tr. 1931) and wrote New Methods of Cell Physiology (1962).

Otto Warburg observed that cancer cells' metabolism is different than the one of normal adult cells. Normal adult cells use a small energy plant located inside them to produce most of their energy needs from oxygen, this is an aerobic process. In contrast, cancer cells rely mainly on the first part of the energy production process dependant on glucose (sugar), this is an anaerobic process. The anaerobic process is called glycolysis.

The paradox is that cancer cells rely on glycolysis even if oxygen is available. This phenomenon is called aerobic glycolysis or the Warburg effect.

Many decades later, this observation was exploited by clinicians to better visualize tumours using PET (positron emission technology) imaging. But it has not been known exactly how tumour cells perform this alternate metabolic feat, nor was it known if this process was essential for tumour growth. Now, two papers appearing in the March 13 (2008) issue of the journal Nature help answer these questions. Led by researchers at Beth Israel Deaconess Medical Centre (BIDMC) and Harvard Medical School, the papers find that the metabolic process that has come to be known as the Warburg effect is essential for tumours' rapid growth, and identifies the M2 form of pyruvate kinase (PKM2), an enzyme involved in sugar metabolism, as an important mechanism behind this process.

The "Warburg Effect" is a unique property of most cancers. The phenomenon is characterized by increased glucose uptake and reliance on glycolysis for ATP production despite available oxygen source.

Cancer Cell Metabolism

Cell

In the above figure, the yellow coloured part is named cytosol, this is where the energy production process starts. At first, glucose molecules are percolating into the cell through the cell membrane by diffusion. You can imagine the glucose molecule in the yellow part of the cell: the cytosol. It doesn't stay free very long, it becomes engaged in a biochemical process to produce what the cells like the best (their favourite food), ATP. This process occurring in the cytosol is named glycolysis. It is not very efficient, only two servings (2 molecules) of ATP are available for all cell metabolism needs. Usually, to satisfy the huge appetite of normal cells, little power plants also nicknamed Mitochondria take a by-product of glycolysis, pyruvate, and convert it into 36 servings!! To accomplish such miracle, mitochondria use oxygen.

Cell Respiration

What Otto Warburg discovered is that most cancer cells rely only on the first part of the energy process: glycolysis. They use glucose to produce their cell food (ATP). Their mitochondria are not involved in the cell food production process. Because they rely on glycolysis which is a less efficient mean of production (only 2 servings of ATP), they need more glucose to satisfy their enormous appetite.

Compared to normal cells which can, from a single molecule of glucose, produce 36 to 38 servings of ATP, cancer cells will need 19 molecules of glucose to produce an equivalent quantity (38 ATP = 2 ATP X 19 glucose). From these numbers we can see that cancer cells will BE huge consumers of glucose to satisfy their sugar crave. This is why some medical imaging techniques can help us locate tumours when they reach a certain size. Radio-active glucose is injected in patients. The Positron Emission Tomography (PET) scan tool is sensible to radio-active material. Since cancer cell will consume 18 to 19 times more glucose than normal cells, they will accumulate more radio-active material as illustrated in the picture below.

Brain Cancer PET scan Shown in the left is a Positron Emission Tomography (PET) scan of a 62 year old man with a brain tumour. The irregular bright yellow and orange area in the lower left portion of the brain indicates the location of the tumour, which metabolizes glucose faster than normal cells.


The Role of Enzymes in Glycolysis

Aerobic Glycolysis - cancer cell
The aerobic glycolysis or the Warburg effect, is thought to be due to the reprogramming of metabolic genes to allow cancer cells to function more like fetal cells and to enable a greater fraction of glucose metabolites to be incorporated into macromolecules synthesis rather than burned to CO2. In other words, glucose is used more for replication than for normal cell metabolism.

Recent research demonstrated that one enzyme makes the whole difference: Pyruvate Kinase. It is an enzyme involved in the last step of the glycolysis process.

Pyruvate kinase exists in two different versions: M1 and M2. The M1 isoform is expressed in most adult tissues; and the M2 isoform is a slice variant of M1 expressed during embryonic development(1).

It has been reported that tumour tissues exclusively express the embryonic M2 isoform of pyruvate kinase(2,3,4).

Given that pyruvate kinase M2 is expressed during embryonic development and in many non-transformed cell lines, M2 expression alone is unlikely to be a transforming event Rather, the presence of of PKM2, may contribute to a metabolism environment that is amenable to cell proliferation.

At the end of the glycolysis process, the enzyme pyruvate kinase help in the final production of two molecules of ATP and one molecule of pyruvate. The pyruvate molecule is then passed to the mitochondria to be transformed into 36 molecules of ATP.

A gatekeeper stands at the front of the mitochondria, it is a mitochondrial enzyme, the pyruvate dehydrogenase (PDH). Without the latter, the pyruvate produced by the glycolysis cannot gets into the highly efficient mitochondria power plant.

Cancer cell Mitochondria

Writing Notes: I need to review the document to edit and most probably add new content. I should get more info on DCA. There is a growing evidence that DCA is very potent for several cancer cases. I saw more and more well documented remission reports in the last months. I should add more content about why glycolysis can contribute to cancer cell proliferation and why some molecules like DCA bring back the natural life cycle. I also need to add several sections about the different stages of tumourigenesis. Barry said that I need to add some content on why active mitochondria lead to apoptosis because this is the DCA active pathway. I think he is right.

references

(1) Jurica M.S et al. The allosteric regulation of pyruvate kinase by fructose-1,6-bisphosphate, Structure 6, 195-210 (1998)

(2) KHeather R. Christofk et al. The M2 slice isoform of pyruvate kinase is important for cancer metabolism and tumour growth. Nature vol. 452|13 March 2008.

(3) Mazurek et al. Pyruvate kinase type M2 and its role in tumour growth and spreading. Semin. Cancer biol. 15, 300-308 (2005)

(4) Dombrauckas et al. Structural basis for tumor pyruvate kinase M2 allosteric regulation and catalysis. Biochemistry 44, 9417-9429 (2005).

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Đây là hình chụp PET Scan của bệnh nhân ung thư giai đoạn di căn (metastasis). Công nghệ chụp PET Scan dc coi là công nghệ chẩn đoán ung thư chính xác và hiệu quả nhất hiện nay. PET Scan là công nghệ chụp xác định sự hấp thụ Glucose của tế bào ung thư.

Bởi ko như chụp MRI hay chụp CT chỉ phát hiện ra khối u ung thư khi nó đã hình thành. Chụp PET Scan xác định được nguy cơ bị ung thư ngay từ trong "trứng nước". Tức như đã từng nói, khối u ung thư có đặc điểm khác biệt đó là khả năng hấp thụ Glucose gấp 20 lần tế bào bình thường.

Do đó, khi ở giai đoạn tiền ung thư - là lúc các tế bào hấp thụ Glucose mãnh liệt để phát triển thành khối u sẽ xảy ra hiện tượng các phần trên cơ thể xuất hiện sự hấp thụ Glucose bất thường.

Như hình minh họa các Dì có thể thấy các phần mầu đỏ đậm là nơi tế bào ung thư lan rộng ra toàn cơ thể và hấp thu đường Glucose rất mãnh liệt, hơn hẳn các khu vực khác của cơ thể.

Chính nhờ việc phát hiện ở giai đoạn chuyển hóa của tế bào ung thư nên sẽ giúp các bác sỹ chẩn đoán bệnh ung thư sớm và đề ra biện pháp chữa trị kịp thời.

Tất nhiên, nhìn vào hình minh họa chúng ta sẽ thấy khi bệnh ung thư đã bước vào giai đoạn di căn thì nó càng hấp thụ Glucose mạnh và có nghĩa rằng bao nhiêu cơm gạo, hoa quả, đường sữa bệnh nhân ăn hàng ngày sẽ đem ra để nuôi tế bào ung thư hết.

Và càng chữa trị thì tế bào ung thư sẽ càng phát triển. Bởi đơn giản phẫu thuật, xạ trị, tiêm hóa chất ko tiêu diệt tận gốc tế bào ung thư. Cắt xẻo chỗ này, mà vẫn cung cấp glucose cho tế bào ung thư thì nó lại lan ra chỗ khác - cái này gọi là di căn (metastasis)

Do đó, giải pháp duy nhất ở đây đó là phải cho bệnh nhân ung thư theo chế độ low carb và high fat. Bằng việc nâng nồng độ ketone trong máu, giảm glucose xuống tối đa[1]. Tế bào ung thư sẽ chết và ko thể phát triển trong môi trường ketosis.

Những ai có ng nhà bị bệnh ung thư có thể theo chế độ high fat của DAS rất đơn giản là ăn các loại rau xanh, củ quả ko tinh bột. Các loại thịt thì ko nên ăn thịt nạc như ức gà, hay ăn thịt bò ( vì ít fat). Mà nên các loại thịt ba chỉ, chân giò, đùi gà ko bỏ da v...v.

Tóm lại là càng high fat thì hiệu quả tiêu diệt tế bào ung thư càng cao.

Bằng cách trên 1 lúc chúng ta sẽ làm 2 việc, 1 là tiêu diệt nguồn thức ăn của tế bào ung thư, 2 là nâng cao sức đề kháng của cơ thể để chống chọi lại tế bào ung thư, cải thiện sức khỏe của bệnh nhân ung thư.

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

SỮa chua hum trước ăn ngon lém, hiehiê, ưhipping xịn có khác

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Tiểu đường không phải là bệnh. Tiểu đường là hệ quả của việc ăn quá nhiều Carbohydrate từ tinh bột, đường kính trong thời gian dài. Làm cho cơ thể bị rối loạn insulin. Từ rối loạn insulin sẽ kéo theo bệnh thận, suy gan.

Như thế ngày nào bệnh nhân tiểu đường còn ăn tinh bột thì ngày đó họ vẫn bị rối loạn insulin và mỗi ngày phải đón nhận 1 cái chết đang tới dần từ việc suy thận, suy gan.

Biện pháp chữa trị tiểu đường hiện nay bằng việc cho bệnh nhân ăn tinh bột, rồi uống thuốc ổn định đường huyết chỉ càng làm cho bệnh nặng thêm và càng phải uống nhiều thuốc --> suy thận càng nhanh mà thôi.

Nếu DAS được áp dụng vào việc chữa bệnh ở VN thì ngay lập những bệnh như cao huyết áp, gout, tiểu đường v...v sẽ biến mất ngay lập tức mà không cần tới bất kì 1 vị bác sỹ, hay bệnh viện, phòng khám, hay 1 vỉ thuốc nào hết.

Bởi tất cã những bệnh trên là do Carbohydrate gây ra. Cứ cắt Carb bệnh sẽ tự khỏi.

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P/S: Dì nào muốn tìm hiểu tại sao DAS có khả năng chữa bệnh tiểu đường, thì xin mời vào link này,
http://on.fb.me/13oxzx0

trong đó có đầy đủ các tài liệu khoa học chuyên môn đề cập tới việc chữa bệnh tiểu đường bằng Low Carb

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Nhiều Dì nghĩ đơn giản là khi theo eDAS 2 thì chỉ cần ăn và nằm ngủ là thành Victoria Secret. Nếu nghĩ vậy thì các Dì đã lầm.

eDAS 2 được thiết kế giúp các Dì giảm từ dạng thừa mỡ, để trở thành ít mỡ, bụng gọn hơn, phẳng hơn. Còn để đạt tới ngưỡng low bodyfat như Victoria Secret thì các Dì phải kết hợp tập luyện.

Ngoài ra muốn giảm nhanh thì thể dục bao giờ cũng cần để đẩy nhanh quá trình trao đổi chất. Còn nếu các Dì bận ko có thời gian tập thể dục, ko sao, cứ theo eDAS 2 đi, từ từ theo thời gian rồi nó sẽ giảm.

Quan trọng là eDAS 2 hướng tới sự thoải mái, dễ dàng giúp các Dì có thể theo được thời gian dài như 1 lifestyle rồi tự nhiên mỡ giảm lúc nào ko hay.

Các Dì ko nên được voi đòi Hai Bà Trưng nhé. Được ăn thoải mái, ko phải tính toán, được relax liên tục, ko phải tập thể dục, lại còn đòi thành VS trong thời gian ngắn thì quả là viễn tưởng đấy heheeh.

Tóm lại DAS luôn khuyên khích các Dì phải tập thể dục để có kết quả tốt nhất. Còn ko tập thì cũng giảm được nhưng phải chấp nhận nó chậm 1 chút nhé.

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Khi down sách eDAS 2 về, đây sẽ là phần đầu tiên mà đa số các DASer sẽ lao vào đọc ( cho dù nó chỉ là phụ lục ) )

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Uống nước hoa quả - 1 trong những sai lầm của nhân loại.

Tiêu đề này nghe có vẻ shock nhưng đó là sự thật.

Nhìn hình minh họa các Dì có thể thấy quả táo bên cạnh một cốc nước táo ép. Ăn quả táo thì tốt ko sao cả, nhưng uống nước táo ép lại sai lầm. Tại sao lại thế ?

Bởi khi chúng ta ăn 1 quả táo thì cùng với đường fructose trong quả táo có kèm theo chất xơ ( là cái bã táo khi người ta ép táo xong rồi vứt đi). Khi ăn 1 quả táo như thế thì do có nhiều chất xơ nên sẽ ngăn cản, làm chậm lại quá trình đường fructose tác động vào đường huyết --> giảm nguy cơ béo phì và tiểu đường.

Vậy nhưng nếu chỉ uống nước ép, coi như chúng ta hấp thụ đường fructose từ quả táo đó 1 cách trực tiếp luôn và do ko có chất xơ nên đường huyết ngay lập tức bị tác động --> béo phì, tiểu đường v...v

Điều này tương tự khi chúng ta uống nước cam ép, hay uống nước ép từ các loại quả ngọt.

Bởi vậy, uống nước hoa quả ép người ta cứ nghỉ là có lợi, thực ra lại rất có hại là ở chỗ đó.

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P/S: Các Dì ko phải lo chuyện uống nước ép từ các loại quả chua như chanh, chanh leo hay nước ép bí đao nọ kia nhé - vì đây là các loại củ quả ko ngọt, chua nên ko có Carb nhé.

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Vấn đề ăn tinh bột và béo phì nó cũng như là hút thuốc lá và bệnh tật vậy. Có nhiều người sức đề kháng tốt, khoẻ mạnh hút thuốc lá mà vẫn sống thọ tới 80,90 tuổi.

Trong khi đó có rất nhiều người sức đề kháng yếu, sức khoẻ kém, hút thuốc tới năm 40 là phổi, họng tan nát hết cả ra rồi.

Như thế nếu chỉ dựa vào những người hút thuốc mà ko bị bệnh rồi nói hút thuốc ko có hại thì nghe có hợp lý ko ?

Tương tự chỉ nhìn vào những người ăn tinh bột ko bị béo phì ( những người gầy ) rồi bảo ăn tinh bột có béo đâu ? Béo phì có phải do tinh bột đâu ?

Thì liệu nghe có lọt tai và hợp logic ko ?

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

https://fbcdn-sphotos-d-a.akamaihd.net/hphotos-ak-xfa1/v/t1.0-9/1000884_481608561917383_1158847170_n.png?Hình minh hoạ ở trên là 1 đoạn trích dẫn từ bài báo mới có nhan đề "Thiếu cơm, cháo cũng bệnh" của ThS.BS TRẦN QUỐC CƯỜNG (Trung tâm Dinh dưỡng TP.HCM), mới được đăng trên hàng loạt báo chí, cả báo giấy, lẫn báo điện tử nhằm mục đích bôi nhọ và xuyên tạc chế độ dinh dưỡng low carb.

Các vấn đề khác Chuối đã phản biện ở bài viết trước. Nên ở bài này Chuối chỉ bàn tới 1 vấn đề căn bản đó là liệu có đúng như Bác sỹ Cường nói là do ko ăn tinh bột thì thiếu những chất như trên ko ?

Xin mời các Dì nhìn tiếp vào 2 bảng thống kê ở dưới, bảng bên trái là hàm luợng dinh dưỡng của gạo, và bên phải là hàm lượng dinh dưỡng của thịt bò.

Xin hỏi xét về vitamin và khoáng chất thì thịt bò với gạo cái nào nhiều hơn ? Đặc biệt là các loại khoáng chất như kẽm, magne, sắt, hay calcium v....v

Ấy là còn chưa kể DAS còn ăn thoải mái các loai rau củ. Liệu có loại vitamin, chất khoáng nào có trong gạo mà ko xuất hiện trong các loại rau xanh, củ quả ít tinh bột và các loại thịt ???

Đây là kiến thức căn bản 1+1=2 của 1 sinh viên ngành Y mà ai cũng biết. Vậy mà ko hiểu vì lí do gì mà bác sỹ Cường lại có thể tuyên bố 1 cách hùng hồn như thế ?

Ở đây chỉ có 2 khả năng:

1 là do đuối lí ko thể phản biện nổi tính khoa học của chế độ low carb. Nên bác sỹ Cường giở trò cả vú lấp miệng em, bằng cách đem cái bằng cấp bác sỹ của mình ra để đổi trắng thay đen với mục đích bôi nhọ low carb bằng mọi giá.

2 là trình độ đào tạo, kiến thức của ngành dinh dưỡng VN quá tồi tệ nên mới đào tạo ra 1 vị bác sỹ có kiến thức kém đến thế.

Thực sự trong thâm tâm Chuối ko bao giờ muốn nó là khả năng 2 vì nếu vậy thì thật là đại hoạ cho sức khoẻ và tương lại của người VN.

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Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

SỐNG KHỎE
Thiếu cơm, cháo cũng bệnh
19/06/2013 06:00 GMT+7
TT - Hiện có nhiều người theo chế độ ăn kiêng rất thấp tinh bột (gần như bỏ cơm, chỉ ăn rau và thịt cá) để giảm cân đôi khi vì lý do thẩm mỹ mà không tham khảo ý kiến bác sĩ.
Tuy có thể phát huy tác dụng nhưng chế độ ăn này tiềm ẩn rất nhiều nguy cơ.


Phóng to
Một khẩu phần ăn chỉ có đạm (thịt gà), chất xơ (dưa leo) mà không có tinh bột - Ảnh: CHÂU ANH
Chế độ ăn rất thấp tinh bột thường chứa dưới 10% năng lượng từ tinh bột và năng lượng còn lại được cung cấp từ chất đạm và chất béo. Tỉ lệ này là rất thấp vì một chế độ ăn bình thường lượng tinh bột chứa khoảng 60-70% năng lượng khẩu phần, thậm chí chế độ ăn cho người đái tháo đường (bị hạn chế tinh bột) cũng chứa ít nhất 55% năng lượng.

Lợi thì có lợi, nhưng…

Do không được cung cấp tinh bột để tạo glucose làm nhiên liệu cho tế bào cơ thể, buộc lòng cơ thể phải phân hủy mô mỡ, cả khối cơ để lấy nguyên liệu tạo ra glucose và thể ceton cho hoạt động hằng ngày. Chế độ ăn này có góp phần giúp giảm cân, ổn định đường huyết ngắn hạn ở vài trường hợp người béo phì và đái tháo đường thông qua nhiều cơ chế như thể ceton giúp giảm cảm giác đói, không có tinh bột làm bữa ăn kém ngon, lượng chất đạm nhiều cũng giúp tăng cảm giác no… Trong y văn, chế độ ăn rất thấp năng lượng cũng giúp ổn định cho bệnh nhi mắc bệnh động kinh nặng không đáp ứng tốt với thuốc, tuy nhiên bệnh nhi sử dụng chế độ ăn này cũng có nguy cơ nhiều tác dụng phụ. Ngoài ra, chế độ ăn rất thấp năng lượng phát huy một phần tác dụng trong bệnh gan nhiễm mỡ.

"Chế độ ăn rất thấp tinh bột không tạo thói quen ăn uống lành mạnh và không giúp kiểm soát cân nặng lâu dài, bền vững"

Tuy nhiên, chế độ ăn rất thấp tinh bột nếu cần thiết chỉ nên sử dụng trong thời gian ngắn (dưới ba tháng) với sự chỉ định và theo dõi y khoa chặt chẽ, vì sử dụng kéo dài có thể phát sinh một số vấn đề về rối loạn chuyển hóa do thiếu tinh bột và thừa đạm, béo trong khẩu phần ăn.

Nếu sử dụng kéo dài, trước tiên bệnh nhân có thể có các triệu chứng như nhức đầu, vọp bẻ, tiêu chảy, yếu mệt, nổi ban… do thiếu các vitamin, khoáng chất có nhiều trong thực phẩm giàu tinh bột, bao gồm vitamin B1, vitamin C, pyridoxin, niacin, riboflavin, acid folic, phospho, sắt, đồng, mangan, chrom. Sử dụng kéo dài chế độ ăn này cũng làm gia tăng nguy cơ bệnh tim mạch do nồng độ chất béo bão hòa và cholesterol cao trong khẩu phần ăn tăng chất béo bù tinh bột, gây cứng thành động mạch, gia tăng LDL cholesterol. Chế độ ăn rất thấp tinh bột cũng được cho rằng làm giảm nồng độ serotonin trong não, dẫn đến các tác dụng phụ về cảm xúc và nhận thức như gia tăng lo lắng, nóng giận, rối loạn cảm xúc, mệt mỏi, trầm cảm, giảm khả năng hoạt động thể lực… Chưa kể, khẩu phần ăn nhiều chất đạm (thịt cá) sẽ gia tăng đào thải canxi qua đường nước tiểu (do làm gia tăng độ acid của nước tiểu), từ đó dẫn đến nguy cơ loãng xương ở người bệnh. Cuối cùng chế độ ăn rất thấp tinh bột gây rối loạn tiêu hóa, táo bón do thiếu tinh bột giúp điều hòa chức năng đường tiêu hóa và giảm khối phân.

Các chế độ ăn giảm thiểu hoặc loại bỏ hoàn toàn tinh bột

Chế độ ăn
Năng lượng từ tinh bột (%)
Năng lượng từ protein (%)
Năng lượng từ chất béo (%)
Chế độ ăn giảm thiểu tinh bột (còn khoảng ½ chén cơm/bữa)
Thấp tinh bột (Zone diet)
40
30
30
Thấp tinh bột, giàu đạm
20-40
30-60
2-30
Thấp tinh bột, giàu béo
20-40
20-30
30-60
Chế độ ăn loại bỏ tinh bột hoàn toàn (loại bỏ hẳn cơm)
Rất thấp tinh bột (Atkins diet)
10
35
50
Rất thấp tinh bột, giàu đạm
0-20
55-65
25-35
Ăn cân bằng dinh dưỡng

Để giúp giảm cân và duy trì cân nặng, mọi người nên theo đuổi chế độ ăn thấp năng lượng nhưng cân bằng dưỡng chất đạm, tinh bột và béo, trong đó lượng tinh bột có thể giảm nhưng không quá cực đoan như trong chế độ ăn rất thấp tinh bột.

Việc kiểm soát tinh bột rất quan trọng, nhưng chúng ta nên hướng đến chuyện tiêu thụ các loại tinh bột có chỉ số đường huyết thấp như gạo lứt (loại gạo còn nhiều cám), các loại khoai (khoai mì, khoai sọ, khoai lang…), bánh mì làm từ lúa mì nguyên hạt, tăng tiêu thụ rau củ quả (giúp làm chậm hấp thu các chất dinh dưỡng, tăng cảm giác no lâu), kiểm soát số lượng thực phẩm ăn vào, tăng tiêu thụ chất đạm từ thực vật, hạn chế thực phẩm giàu béo, giàu cholesterol.

Kinh nghiệm cho thấy nếu được tư vấn kỹ cũng như tái khám thường xuyên trong quá trình điều trị, người dư cân, béo phì sẽ đạt được mục tiêu và thành công trong việc điều trị. Mục tiêu trong điều trị béo phì về bản chất không phải là việc sụt bao nhiêu cân nặng mà là tăng cường sức khỏe, hạn chế biến chứng do béo phì gây ra, do đó không có lý do gì theo đuổi một chế độ ăn hay một cách giảm cân nào đó chỉ có tác dụng giảm cân nặng nhưng lại sinh ra nhiều rối loạn chuyển hóa và tiềm ẩn nhiều nguy cơ bệnh tật khác cho cơ thể.

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Cancer Loves Sugar




Every doctor learned back in medical school all about Otto Warburg's discovery; a discovery of humongous proportions, because way back in the thirties Otto discovered the main biochemical cause of cancer, or what differentiates a cancer cell from a normal, healthy cell. So big a discovery was this, that Otto Warburg was awarded the Nobel Prize.

Cancer has only one prime cause. It is the replacement of normal oxygen respiration of the body's cells by an anaerobic [i.e., oxygen-deficient] cell respiration. -Dr. Otto Warburg

But what else does Warburg's discovery tell us. First off, it tells us that cancer metabolizes much differently than normal cells. Normal cells need oxygen. Cancer cells despise oxygen. In fact, oxygen therapy is a favorite among many of the alternative clinics we've researched.

Another thing this tells us is that cancer metabolizes through a process of fermentation.

If you've ever made wine, you'll know that fermentation requires sugar.

The metabolism of cancer is approximately 8 times greater than the metabolism of normal cells.

Okay, so here is what we can put together knowing the above: The body is constantly overworked trying to feed this cancer. The cancer is constantly on the verge starvation and thus constantly asking the body to feed it. When the food supply is cut off, the cancer begins to starve unless it can make the body produce sugar to feed itself.

The wasting syndrome, cachexia, is the body producing sugar from proteins (you heard it right, not from carbohydrates or fats, but from proteins) in a process called glycogenesis. This sugar feeds the cancer. The body finally dies of starvation, trying to feed the cancer.

Now, knowing that one's cancer needs sugar, does it make sense to feed it sugar? Does it make sense to have a high carbohydrate diet?

The reason Food Therapies for cancer even exist today (beyond the fact that they work) is because someone once saw the connection between sugar and cancer. There are many food therapies, but not a single one allows many foods high in carbohydrates and not a single one allows simple sugars, BECAUSE SUGAR FEEDS CANCER.

Why doesn't your physician tell you this? Hard to tell. Maybe your doctor feels it is his job to cure your cancer, not yours. Maybe because your doctor learned about Warburg, but never put 2 + 2 together; never put nutrition into the equation. Maybe because your physician didn't study nutrition. Heck, as late as 1978, the AMA's official position (found in the Congressional Record) was that nutrition had nothing to do with disease.

However, those who've paid attention to this sugar craving cancer stuff have come up with some remarkable therapies for cancer. Laetrile is just one: the glucose in laetrile is dragged into the cancer cell because of its need for sugar. Hydrazine Sulfate, which stops the process of glycogenesis in greater than 50% of all patients with cachexia is another.

A Reader's Contribution

Be aware that refined carbohydrates are turned rapidly into sugar (mainly glucose) in the stomach to produce what body builders and others refer to as a “sugar rush”. This prompts the emergency production of insulin to do everything possible to keep blood sugar levels under control including converting excess sugar to fat; all in order to prevent blood sugar from reaching dangerously high levels.

The mechanism behind the sugar rush is simple; after refining, the carbohydrate molecules are much more accessible and of greater surface area than when they are attached to their associated fibre (which is removed during the milling process). The milling process breaks the carbohydrate down into much smaller particles than happens during normal mastication, and thus the increased surface area greatly speeds up their conversion to sugar. By this process, white flour, white sugar and even fruit juices feed cancer.

A little known additional consequence of this sugar rush is that it reverses the normal nutrient/blood flow to the teeth which normally occurs from the inside out. However, the hydraulic pressure inside the teeth reduces to zero, allowing harmful bacteria to attach to the exterior of the teeth and begin their metabolic chemistry which dissolves the enamel and underlying tissues.
Ron More, New Zealand, www.prestogel.co.nz

A while back (2004), at the University of Minnesota, they were experimenting with a chemotherapy delivered in a "smartbomb." Here's the scoop: the drug is wrapped in a coating that stays intact as it travels through the body, that is until it reaches a location of no oxygen. When it reaches this "no oxygen" location, the coating falls apart releasing the chemotherapy to destroy the cancer, because the only place in your body where there is no oxygen is the cancer site.

Laetrile, as noted above, is a natural smartbomb; though not approved by the FDA.

The results of the 2004 UofMN study must have been have been buried. Nothing exists on it. There are, however, lots of recent articles on cancer smart bombs:

http://www.cbsnews.com/8301-504763_...argeting-disease-leaving-healthy-cells-alone/

http://www.huffingtonpost.co.uk/2012/07/15/cancer-treatment-smart-bomb_n_1674085.html

http://www.sciencedaily.com/releases/2012/09/120914135327.htm

Then there are the food therapies: aimed at starving cancer. Knowing what cancer loves, the cancer patient avoids them. Cancers likes cooked foods over raw (cooking destroys enzymes and heat sensitive vitamins), so check out our article on the cancer diet. And, do not forget, cancer loves sugar. If you dislike your cancer, then don't feed it.

Further Reading:

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Is Sugar Toxic?

Kenji Aoki for The New York Times
By GARY TAUBES
Published: April 13, 2011
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On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

Q. and A With Gary Taubes
The author answered reader questions on the Well blog.
Multimedia
What the average American consumes in added sugars:

Graphic
High-Fructose Corn Syrup Consumption

Graphic
Sugar Consumption
Related

Sweet and Vicious (May 1, 2011)
Times Topic: Sugar
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Kenji Aoki for The New York Times
Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.


Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (v.titunik-MagGroup@nytimes.com).

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb

Sau Tết c bon che n vậy giờ k thể das nổi

 

Ðề: ĐỒ ĂN LOWCARB (Sữa chua, caramen,thạch,bánh mỳ hạt lanh,bánh cuộn,các loại hạt lowcarb


Đây là bảng thống kê số đường kính tính theo đầu người, thì như hình các Dì có thể nhìn thấy. [1].

Người Nhật trung bình một năm chỉ ăn khoảng 16,9 kg đường (2000) và 17,8 kg đường (2011) so sánh với các nước xung quanh như Thái Lan (37,8 kg), Australia (57,8) thì người Nhật ăn rất ít đường kính.

Chỉ có Trung Quốc là ăn ít đường kính hơn Nhật 10,7 kg. Nhưng do Trung Quốc dân số đông phân bố rộng nên nạn béo phì tập trung ở các đô thị nơi mà người dân đủ điều kiện ăn uống tiêu thụ nhiều loại đồ ngọt, còn đại đa số dân TQ sống ở các vùng xa xôi hẻo lánh, nghèo thì ko có điều kiện ăn nhiều các loại bánh trái, đường kính, đồ ngọt như ở thành thị.

Cái này nó giống như 10 thằng thì 1 thằng ăn 9 con con gà, còn lại 9 thằng thì chỉ ăn 1 con gà, nhưng tính trung bình ra thì mỗi thằng vẫn ăn 1 con gà.

Còn Nhật thì lại khác do mức sống của họ cao và ko chênh lệch giầu nghèo nhiều nên mức tiêu thụ đường kính của họ được phân bố đều ra, chứ ko như TQ.

Đây là 1 trong những lí do vì sao mà người Nhật có tỉ lệ béo phì thấp so với các nước xung quanh trong khu vực. Bởi họ ăn ít đồ ngọt và đường kính.

- Ad Chuối -