Dietary Protein, Not Sugar, Promotes the Growth of Cancer

Some researchers in Bel­gium just did an inter­est­ing study about how yeast cells use sug­ar. This study helps to explain why yeast cells mul­ti­ply rapid­ly when they have plen­ty of sug­ar. The results of their study could also explain why some can­cer cells also mul­ti­ply rapid­ly. How­ev­er, this study does not mean that sug­ars and starch­es in the diet are a prob­lem. In fact, high-car­bo­hy­drate diets actu­al­ly help to pro­tect against many can­cers. Rather, the study explains why can­cer cells with abnor­mal sug­ar metab­o­lism might behave like yeast cells.

Many Cancer Cells Have an Abnormal Metabolism

Since the 1920s, sci­en­tists have known that many can­cer cells don’t use oxy­gen to burn sug­ar, even when plen­ty of oxy­gen is avail­able. By the 1950s, it was clear that tumors that are most like­ly to use anaer­o­bic (no-oxy­gen) metab­o­lism tend to be the most aggres­sive. Unfor­tu­nate­ly, the reporters who have been cov­er­ing this study for the pop­u­lar press do not under­stand what the study is about or what its results real­ly mean.

Many of the reporters have false­ly con­clud­ed that the study shows that some­thing in sug­ar is some­how caus­ing can­cer. As a result, they are urg­ing peo­ple to avoid eat­ing car­bo­hy­drates. But if peo­ple fol­low that advice, they would actu­al­ly increase their risk of ear­ly death. If peo­ple avoid car­bo­hy­drates, they will end up eat­ing more fat and more ani­mal pro­tein. High-fat diets increase your risk of heart attacks. Also, diets that are high in ani­mal pro­tein increase your risk of dying of can­cer.

Many Cancer Cells Have an Abnormal Metabolism

The Bel­gian study tells us some­thing that is inter­est­ing to cell biol­o­gists and to can­cer researchers but is of no inter­est to the gen­er­al pub­lic. Since the 1920s, it has been clear that many can­cer cells pre­fer to use anaer­o­bic metab­o­lism, even when they have no short­age of oxy­gen. This pref­er­ence is called the War­burg effect. Sci­en­tists have also known since the 1950s that the can­cers that exhib­it the War­burg effect tend to be more aggres­sive. Back in 1956, Otto Hein­rich War­burg, MD, PhD, argued that the can­cer cells’ abnor­mal fail­ure to use oxy­gen was the under­ly­ing cause of can­cer. This idea is called the War­burg Hypoth­e­sis.

Sci­en­tists now know that the can­cer cells’ abnor­mal metab­o­lism is a result of the gene muta­tions that caused them to become malig­nant. How­ev­er, the Bel­gian study actu­al­ly shows that the War­burg hypoth­e­sis was not far off the mark. The Bel­gian researchers showed how the War­burg effect real­ly might cause the can­cer to be more aggres­sive. A sub­stance that might build up in a can­cer cell, as a result of the cell’s abnor­mal metab­o­lism, can acti­vate chem­i­cal sig­nals that would pro­mote the growth and divi­sion of that cell. The Bel­gian study is inter­est­ing because some of the sig­nal­ing chem­i­cals are prac­ti­cal­ly the same in human cells as in yeast.

How Cells Burn Sugar

To under­stand the War­burg effect, you need to know how cells burn sug­ar. Your body’s favorite fuel is a sug­ar called glu­cose. Glu­cose is the main sug­ar in your blood­stream.

The Glycolytic Pathway

When we eat sucrose (table sug­ar), the mol­e­cule of sucrose will be split into a mol­e­cule of glu­cose and a mol­e­cule of fruc­tose. When we digest starch, we break it down to mol­e­cules of glu­cose. Cells even­tu­al­ly con­vert both glu­cose and fruc­tose into a com­pound called fructose-1,6-bisphosphate. After a few more chem­i­cal changes, the sug­ar mol­e­cule is split into two pieces. This split­ting is called gly­col­y­sis.

To split the sug­ar mol­e­cule, the cell must make an invest­ment of ener­gy. The cell’s imme­di­ate­ly usable ener­gy is stored main­ly in a high-ener­gy mol­e­cule called adeno­sine triphos­phate (ATP). To split the sug­ar mol­e­cule, the cell must con­vert two mol­e­cules of ATP to a low­er-ener­gy mol­e­cule called adeno­sine diphos­phate (ADP).  But at the end of the gly­col­y­sis process, the cell will have two mol­e­cules of pyru­vate and will have con­vert­ed four mol­e­cules of ADP to ATP. So the cell will have a net gain of two ATP mol­e­cules.

The gly­col­y­sis process will also con­vert a coen­zyme called nicoti­namide ade­nine din­u­cleotide (NAD+) to its reduced form (NADH). Two mol­e­cules of NAD+ get reduced to NADH for every mol­e­cule of glu­cose that is con­vert­ed to pyru­vate. No oxy­gen mol­e­cules are involved in the process of gly­col­y­sis. For this rea­son, gly­col­y­sis can take place even in a low-oxy­gen (anaer­o­bic) envi­ron­ment.

Ferment or Burn the Pyruvate?

So what hap­pens to the pyru­vate? The pyru­vate can under­go two dif­fer­ent kinds of metab­o­lism. In a low-oxy­gen envi­ron­ment, many kinds of cells will recoup their lost NAD by con­vert­ing the pyru­vate to alco­hol or lac­tic acid. For exam­ple, yeast cells in a wine cask turn the glu­cose from grape juice into alco­hol. Also, mus­cle cells pro­duce some lac­tic acid dur­ing intense (anaer­o­bic) exer­cise.  But in a high-oxy­gen envi­ron­ment, many kinds of cells can do aer­o­bic metab­o­lism. They will use oxy­gen to break the pyru­vate down com­plete­ly into car­bon diox­ide and water. Aer­o­bic bac­te­ria can do this. So can the mito­chon­dria inside the cells of plants, fun­gi, and ani­mals.

From an ener­gy stand­point, aer­o­bic metab­o­lism is far more effi­cient. Aer­o­bic metab­o­lism yields a net gain of 30 to 32 mol­e­cules of ATP for each mol­e­cule of glu­cose, as opposed to the net gain of only 2 mol­e­cules of ATP that the cell gets from anaer­o­bic metab­o­lism of a mol­e­cule of glu­cose. For the body as a whole, anaer­o­bic metab­o­lism is an even worse deal. When a cell does anaer­o­bic metab­o­lism, it pro­duces lac­tic acid. Then, the liv­er must invest six mol­e­cules of ATP to con­vert the lac­tic acid back to glu­cose. As a result, your body has a net loss of 4 mol­e­cules of ATP for every mol­e­cule of glu­cose that under­goes anaer­o­bic metab­o­lism in your mus­cles.

The Really Bad Cancer Cells Are Anaerobic

War­burg knew that many can­cer cells pre­fer to use anaer­o­bic metab­o­lism, even when they have plen­ty of oxy­gen. He showed us that the most aggres­sive can­cers were most like­ly to pre­fer anaer­o­bic metab­o­lism. These find­ings help to explain why so many can­cer patients lose weight so fast.

For every mol­e­cule of glu­cose that a can­cer cell uses, the can­cer cell gets a net gain of 2 mol­e­cules of ATP. Mean­while, the liv­er has to invest 6 mol­e­cules of ATP to con­vert the lac­tic acid pro­duced by the can­cer cell back into glu­cose. So besides los­ing glu­cose to the tumor, the body has to burn calo­ries to clean up the mess that the tumor is mak­ing. If the body has many can­cer cells, the liv­er will use up a lot of calo­ries to clean up the mess. The result is a rapid weight loss called can­cer cachex­ia (pro­nounced ka-kex-ia). Cachex­ia comes from the Greek words for “bad con­di­tion.”

What the Belgian Study Teaches Us

The Bel­gian study could explain why the War­burg effect hap­pens. It involves a set of intra­cel­lu­lar sig­nals that are prac­ti­cal­ly the same in yeast cells as in human cells.

When yeast cells have plen­ty of glu­cose or fruc­tose, they make a lot of fructose-1,6-bisphosphate. This fructose-1,6-bisphosphate then acti­vates a sig­nal­ing pro­tein called Ras. Ras encour­ages the yeast cell to grow and divide faster.

In a nor­mal human cell, the process­es for burn­ing sug­ar are tight­ly con­trolled. But in a can­cer cell, these con­trols might be defec­tive. One pos­si­ble result is an abnor­mal buildup of fructose-1,6-bisphosphate inside the cell. Unfor­tu­nate­ly, this extra fructose-1,6-bisphosphate would acti­vate Ras. The acti­vat­ed Ras would then tell the cell to grow and mul­ti­ply. This could explain why the can­cers that have abnor­mal car­bo­hy­drate metab­o­lism are like­ly to be more aggres­sive.

The results of the Bel­gian study could explain why some defec­tive cells mul­ti­ply fast. How­ev­er, it tells us noth­ing about how our food choic­es affect our health. To answer that ques­tion, we need to look at oth­er kinds of stud­ies.

High-Carbohydrate Diets Help Protect  Against Cancer

As T. Col­in Camp­bell, PhD, explained in The Chi­na Study, can­cer involves two basic prob­lems. The first prob­lem is can­cer ini­ti­a­tion, which means that one or more cells have become malig­nant. The things that cause can­cer ini­ti­a­tion are called car­cino­gens. Can­cer pro­mot­ers, in con­trast, are things that help the exist­ing can­cer cells sur­vive and mul­ti­ply. By avoid­ing car­cino­gens, you can reduce the risk that a can­cer will start in your body. If you also avoid can­cer pro­mot­ers, then your can­cer cells might grow so slow­ly that you nev­er even know they are there.

Some drugs can pro­mote can­cer, either by sup­press­ing the immune sys­tem or by encour­ag­ing can­cer cells to mul­ti­ply faster. Some foods can also pro­mote can­cer. Camp­bell has explained that ani­mal-source foods are can­cer pro­mot­ers.  You can make some can­cers in lab­o­ra­to­ry ani­mals grow faster by feed­ing them ani­mal pro­tein. You can switch the growth of those can­cers off by tak­ing the ani­mal pro­tein out of the diet.  In human beings, a high-car­bo­hy­drate, plant-based diet works in sev­er­al ways to reduce your risk of dying of can­cer.  It might even sup­press a can­cer with abnor­mal sug­ar metab­o­lism.

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