Free Shipping on All Orders $75 Or More! Ends Soon.

Your Trusted Brand for Over 35 Years

Life Extension Magazine

<< Back to January 2018

Milk Thistle May Help Protect Against Second-Hand Cigarette Smoke

January 2018

By Roger Price

Smoking is a huge cause of preventable death1 and has a devastating reach of deadly consequences from lung cancer, heart disease, stroke, osteoporosis, and to cancers in many parts of the body.2,3

Even more insidious is the exposure to second-hand smoke. That is, the involuntary inhalation of smoke from a burning cigarette or a smoker exhaling.

According to the Centers for Disease Control, “there is no risk-free level of second-hand smoke exposure; even brief exposure can be harmful to health.”4

In fact, second-hand smoke has been cited as a carcinogen by the US Environmental Protection Agency and the National Toxicology Program.5

Second-hand smoke contains a long list of dangerous poisonous chemicals and gases, including carbon monoxide (found in car exhaust), butane (used in lighter fluid), hydrogen cyanide (used in chemical weapons), ammonia (used in household cleaners), and toluene (found in paint thinners).

Additionally, second-hand smoke contains arsenic (used in pesticides), lead (formerly found in paint), and cadmium (used to make batteries).6

This article reveals a novel way to potentially help protect against the adverse impact of second-hand cigarette smoke.

When nonsmokers are exposed to second-hand smoke, they may as well be smoking since they are breathing many of the same cancer-causing chemical as do smokers.5

Just living with a smoker can dramatically increase the risk of lung cancer.7

Approximately 2,500,000 nonsmokers have died from health problems caused by second-hand smoke since 1964.4 (That’s 2.5 million nonsmokers who died from other people’s smoking.)

But by far, smoking—and second-hand smoke—is the biggest risk factor for developing chronic obstructive pulmonary disease (COPD).8

In the US, COPD is the third leading cause of death.9,10 Worldwide, the disease kills about 3 million people annually—roughly twice the number who die from lung cancer.

Cigarette smoke, which contains thousands of toxic compounds and chemicals, causes the airways to become inflamed and damaged.11,12 Although the symptoms of COPD can be treated, little could be done to reduce smoke-induced lung inflammation or to prevent the changes associated with COPD.

Until now.

Three recent studies reveal that silymarin, a compound derived from milk thistle, has protective properties that can help reduce smoke-induced inflammatory responses—while also preventing the inflammation-induced damage to the airways that produces COPD.

This information is essential for the 12% of Americans over 65 who still smoke despite the known risks,13 as well as for the millions more whose health is threatened by exposure to second-hand smoke.

COPD – The Most Ignored Smoking-Related Risk

Most people think of lung cancer as smoking’s biggest health risk. But while lung cancer strikes about 222,500 people each year,14 in the United States that figure is dwarfed by the nearly 12 million victims of COPD.15

Preventing COPD can help prevent lung cancer, since COPD is a major risk factor for developing the disease.16,17

If you’ve ever known someone who suffers from it, you know how unpleasant COPD is. It’s a progressive condition that makes it hard to breathe, although in the early stages there may be only mild symptoms. COPD includes chronic bronchitis, emphysema, and sometimes asthma.9,18,19 As the condition progresses, everyday activities like getting dressed can become extremely difficult.

COPD is commonly due to exposure to tobacco smoke, which causes chronic inflammation in the airways (called the bronchi) that deliver air in and out of the lungs. Over time, this results in fibrosis, a form of scarring that narrows the bronchi substantially, making breathing increasingly difficult.20-22

Oxygen therapy is the primary means of reducing the death risk from COPD. Inhaled medications such as bronchodilators and corticosteroids may improve symptoms, but they have no impact on mortality.23 This leaves many COPD sufferers with nothing much but palliative care and the certainty of an untimely death.

Making matters worse, because COPD contributes to chronic inflammation throughout the body, it also increases the risk of other inflammation-linked diseases.

People with COPD have markedly elevated risks of lung cancer, cardiovascular disease, and stroke.17,23-26

COPD is closely associated with frailty (a syndrome that includes muscular weakness and balance disturbances), which is itself associated with risk of early death.27,28 COPD is also associated with osteoporosis, anxiety, malnutrition, and depression.23

Smoking’s Deadly Inflammatory Consequences
Smoking’s Deadly Inflammatory Consequences

Tobacco use, mainly cigarette smoking, is the leading cause of preventable death in America.34 It is a major contributor to COPD, and it greatly increases cardiovascular disease risks and visual impairment, largely through its promotion of inflammation throughout the body.22,23,34

Both the smoke itself (which is really just a cloud of tiny particles of burned tobacco, added chemicals, and paper), and the chemical nicotine that it contains, contribute to chronic smoke-associated inflammation.35 And inflammation, as we now know, contributes to virtually every age-related chronic disease, including those as diverse as cancer, osteoporosis, and Alzheimer’s disease.16,17,28,31,36,37

Research highlights the impact of nicotine on inflammatory changes in blood vessels that eventually produce arterial thickening, stiffening, and reduced blood flow to major organs—the underlying factors of cardiovascular disease.35 Inflammatory changes damage endothelial function,24,33,36 which prevent arteries from being able to regulate blood flow and pressure, while also making platelets and vessel walls “stickier.” These processes increase the likelihood of a catastrophic blood clot that triggers a heart attack or stroke.

As we’ve seen in this article, extracts of milk thistle—silymarin and its chief component, silibinin—have a powerful anti-inflammatory effect that can help protect against smoke-induced inflammation and its consequences.

The Dangers of Second-Hand Smoke

The Dangers of Second-Hand Smoke  

Passive smoking occurs when a person is exposed to someone else’s tobacco smoke. Nonsmokers who are exposed to cigarettes are still breathing the same harmful particles and chemicals that make smoking so harmful to smokers.29

Studies show that passive smoking raises the risk of lung cancer (and other cancers), heart attacks, stroke, depression, and frailty—all of which increase the risk of an early death. Living with a smoker can increase the risk of lung cancer by as much as 30%.7

In fact, more than 20% of people with COPD don’t smoke.30

Whether you’re the one doing the smoking or not, the bottom line is there is no safe level of exposure to cigarette smoke. But there is good news. While it can still be difficult to avoid others’ smoke, there is something you may do to help protect yourself from its harmful effects.

Silymarin has been shown to reduce the inflammation caused by smoke exposure. This can possibly enable you to protect yourself, if not from the smoke itself, then at least from some of its deadly consequences.

How Silymarin may Help Protect Against COPD

Silymarin and its main component, silibinin, are the most important bioactive constituents of milk thistle. Extracts from milk thistle have been used for more than 2,000 years as traditional therapies for liver diseases. They are still used for that purpose today.31

The reason silymarin constituents are beneficial in liver disease is largely because of their ability to combat chemical stress and inflammation—both of which contribute to liver diseases such as nonalcoholic fatty liver disease (NAFLD), cirrhosis, and some types of hepatitis.

More recently, scientists have started to explore silymarin’s anti-inflammatory properties in other diseases as well, broadening the scope of potential uses for this ancient remedy. These studies have highlighted silymarin’s powerful ability to combat the smoke-induced causes of COPD.

Three of the most recent silymarin studies offer, for the first time, real hope for COPD sufferers, for whom few therapies can change the inflammation-driven course of the disease.

Study #1

In the first study, mice were exposed to the equivalent of 1.5 packs of cigarette smoke per day for four weeks.20

Even though four weeks are much less than the lifetime of exposure most older COPD patients have experienced, this limited smoke exposure still produced profound increases in inflammation in the mice. This was demonstrated by high levels of inflammatory cell infiltration, thickening of airway walls, and obstruction of their airways—all features of COPD in humans.20

But when the animals were pretreated with silymarin, all of the inflammatory changes caused by the cigarette smoke were sharply reduced.20 There were also significant reductions in the secretion of pro-inflammatory signaling molecules (cytokines) such as TNF-alpha, IL-1beta, and IL-8.

Smoking is also known to decrease one of the body’s most protective enzymes, called superoxide dismutase (SOD). SOD is one of the body’s primary internal defenses, and plays a critical role in reducing oxidative stress and inflammation.

This study showed that the higher dose of silymarin prevented the decreases in SOD caused by cigarette smoke—a powerful demonstration of silymarin’s natural healing properties.20

Study #2

The second recent study was performed by the same group of researchers, this time using human bronchial cells in culture in order to shed light on how silymarin produces such dramatic anti-inflammatory benefits.21 They found that silymarin reduced the secretion of inflammatory cytokines caused by cigarette smoke by modulating a signaling pathway called ERK MAPK, which is a natural cellular stress-response system that induces inflammation.21

These anti-inflammatory actions were so impressive that the researchers suggested that silymarin could be an “ideal agent” for treating inflammatory lung diseases like COPD.

Study #3

The most recent study, published in mid-2017, is possibly the most exciting. Not only did it confirm silymarin’s ability to reduce inflammation in the bronchi—it also revealed that it reduced the damage caused by the inflammation.

For this study, researchers exposed mice to even smaller amounts of cigarette smoke—equivalent to just one hour of cigarette smoke per day (that’s eight cigarettes) for four weeks.22 The mice also received a powerful toxin to boost the inflammatory response.

Just before the daily hour of cigarette smoke exposure, mice received either a high or low oral dose of silibinin (also known as silybin), an active component of silymarin.22

This study demonstrated that both doses of silibinin sharply reduced the inflammatory changes in the bronchi in a fashion similar to the other studies.22

In addition, the researchers found that silibinin significantly suppressed the cigarette smoke-induced scarring and fibrosis typical of humans with COPD. This protective action occurred in part by silibinin’s ability to directly inhibit the expression of TGF beta-1, a protein that can increase local inflammation, and whose expression is increased by inflammation and smoke.

These three studies are the first demonstration of a therapy that can reduce the life-threatening scarring in smokers’ lungs that severely compromises normal air exchange. This lung scarring eventually makes breathing so difficult that victims often have difficulty with even the simplest tasks such as speaking, eating, or drinking.

The Future of Silymarin

The growing realization that chronic inflammation is one of the deadliest effects of smoking32 suggests that silymarin could be a useful preventive agent for anyone who is, or ever has been, exposed to cigarette smoke.

As an added benefit, another study has demonstrated intriguing evidence that silymarin could have a powerful preventive effect on bladder cancer, which is associated with tobacco smoke exposure.33

With increasing evidence that silymarin’s anti-inflammatory properties extend well beyond its traditional role as a liver tonic, it seems likely that this is just the tip of the iceberg of silymarin’s benefits for the body.



With no medical cure, and only palliative therapy available, COPD sufferers have been condemned to premature death.

New studies demonstrate that extracts of the milk thistle—silymarin and its chief component, silibinin—markedly reduce the disastrous impact of chronic, smoke-induced inflammation on lung tissue. This results in potential protection against the kind of physical and biochemical changes seen in COPD.

Silymarin’s anti-inflammatory effects may also have benefit in other smoking-related disorders, given the important impact of inflammation on cardiovascular disease and cancer.

Anyone exposed to tobacco smoke (whether directly or indirectly) may consider supplementation with milk thistle, in the hopes of evading COPD, heart attacks, strokes, and even some cancers.

And at this point “hope” is about all we can expect as the deadly effect of second-hand smoke, and how to prevent it from killing those unintentionally exposed, has yet to be fully documented.

With regular milk thistle supplementation, it may finally be possible to provide some genuine protection against this powerful environmental threat.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.


  1. Available at: Accessed October 26, 2017.
  2. Available at: Accessed October 23, 2017.
  3. Available at: Accessed October 23, 2017.
  4. Available at: Accessed October 26, 2017.
  5. Available at: Accessed October 26, 2017.
  6. Available at: Accessed October 26, 2017.
  7. Available at: Accessed October 23, 2017.
  8. Laniado-Laborin R. Smoking and chronic obstructive pulmonary disease (COPD). Parallel epidemics of the 21 century. Int J Environ Res Public Health. 2009;6(1): 209-24.
  9. Available at: Accessed October 23, 2017.
  10. Available at: Accessed October 23, 2017.
  11. Available at: Accessed October 23, 2017.
  12. Talhout R, Schulz T, Florek E, et al. Hazardous compounds in tobacco smoke. Int J Environ Res Public Health. 2011;8(2):613-28.
  13. Kaplan MS, Newsom JT, McFarland BH. Older adults’ contact with health practitioners: is there an association with smoking practices? J Gerontol A Biol Sci Med Sci. 2002;57(6):M343-6.
  14. Available at: Accessed 23 June, 2017.
  15. Available at: Accessed 23 June, 2017.
  16. Lee S, She J, Deng B, et al. Multiple-level validation identifies PARK2 in the development of lung cancer and chronic obstructive pulmonary disease. Oncotarget. 2016;7(28):44211-23.
  17. Yang IA, Relan V, Wright CM, et al. Common pathogenic mechanisms and pathways in the development of COPD and lung cancer. Expert Opin Ther Targets. 2011;15(4):439-56.
  18. Available at: Accessed October 23, 2017.
  19. Available at: Accessed October 23, 2017.
  20. Li D, Xu D, Wang T, et al. Silymarin attenuates airway inflammation induced by cigarette smoke in mice. Inflammation. 2015;38(2):871-8.
  21. Li D, Hu J, Wang T, et al. Silymarin attenuates cigarette smoke extract-induced inflammation via simultaneous inhibition of autophagy and ERK/p38 MAPK pathway in human bronchial epithelial cells. Sci Rep. 2016;6:37751.
  22. Ko JW, Shin NR, Park SH, et al. Silibinin inhibits the fibrotic responses induced by cigarette smoke via suppression of TGF-beta1/Smad 2/3 signaling. Food Chem Toxicol. 2017.
  23. Nazir SA, Erbland ML. Chronic obstructive pulmonary disease: an update on diagnosis and management issues in older adults. Drugs Aging. 2009;26(10):813-31.
  24. Garcia-Esquinas E, Navas-Acien A, Rodriguez-Artalejo F. Exposure to secondhand tobacco smoke and the frailty syndrome in US older adults. Age (Dordr). 2015;37(2):26.
  25. Messner B, Bernhard D. Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arterioscler Thromb Vasc Biol. 2014;34(3):509-15.
  26. Windsor C, Herrett E, Smeeth L, et al. No association between exacerbation frequency and stroke in patients with COPD. Int J Chron Obstruct Pulmon Dis. 2016;11:217-25.
  27. Park SK, Richardson CR, Holleman RG, et al. Frailty in people with COPD, using the National Health and Nutrition Evaluation Survey dataset (2003-2006). Heart Lung. 2013;42(3):163-70.
  28. Nyunoya T, Mebratu Y, Contreras A, et al. Molecular processes that drive cigarette smoke-induced epithelial cell fate of the lung. Am J Respir Cell Mol Biol. 2014;50(3):471-82.
  29. Available at: Accessed October 23, 2017.
  30. Available at: Accessed October 23, 2017.
  31. Park JW, Shin NR, Shin IS, et al. Silibinin Inhibits Neutrophilic Inflammation and Mucus Secretion Induced by Cigarette Smoke via Suppression of ERK-SP1 Pathway. Phytother Res. 2016;30(12):1926-36.
  32. Lee J, Taneja V, Vassallo R. Cigarette smoking and inflammation: cellular and molecular mechanisms. J Dent Res. 2012;91(2):142-9.
  33. Tyagi A, Raina K, Singh RP, et al. Chemopreventive effects of silymarin and silibinin on N-butyl-N-(4-hydroxybutyl) nitrosamine induced urinary bladder carcinogenesis in male ICR mice. Mol Cancer Ther. 2007;6(12 Pt 1):3248-55.
  34. Zhang X, Kahende J, Fan AZ, et al. Smoking and visual impairment among older adults with age-related eye diseases. Prev Chronic Dis. 2011;8(4):A84.
  35. Wang CN, Yang GH, Wang ZQ, et al. Role of perivascular adipose tissue in nicotineinduced endothelial cell inflammatory responses. Mol Med Rep. 2016;14(6):5713-8.
  36. Stringer KA, Freed BM, Dunn JS, et al. Particulate phase cigarette smoke increases MnSOD, NQO1, and CINC-1 in rat lungs. Free Radic Biol Med. 2004;37(10):1527-33.
  37. Oschman JL. Chronic disease: are we missing something? J Altern Complement Med. 2011;17(4):283-5.