Peter Attia MD#162 - Sarah Hallberg, D.O., M.S.: Treating metabolic disease, & a personal journey through cancer
CHAPTERS
- 0:02 – 8:22
Why Fatty Acid Distribution Matters, and Sarah's Path to Carbohydrate Restriction
Peter Attia opens by asking why Sarah Hallberg cares about how dietary carbohydrate and fat shape fatty acids in the body. She explains her years of giving low-fat advice, her frustration in primary care, and her discovery of carbohydrate restriction when asked to build an obesity program.
- •Hallberg says fatty acids are underdiscussed because they are confusing, and "you are what you eat" is a worn-out idea
- •She spent about a decade advising low-calorie, low-fat diets and watched patients get worse
- •Anger at primary care led her to an obesity program, where she read the literature and found carbohydrate restriction
- •Her clinic saw type 2 diabetes resolve, with patients coming off insulin at striking rates
- 8:22 – 16:58
Institutional Pushback, Research, and the Virta Trial
Attia asks about the patient mix and resistance within her institution. Hallberg describes presenting the evidence to every department, getting a unanimous committee vote, and then moving into research that led to a large five-year trial of nutritional ketosis.
- •She presented a 15-minute slide talk to departments and met no pushback
- •A quality committee amendment to offer carbohydrate restriction to patients with metabolic disease passed unanimously
- •A chance meeting with Steve Phinney led to funding for a large trial of nutritional ketosis
- •Other specialists said the diet works but nobody can stay with it, which she disputed from her own practice
- •The eighth paper from the trial, on prediabetes, was published the day of the recording
- 16:58 – 27:47
Prediabetes, Metabolic Syndrome, and Health Equity
The conversation turns to what prediabetes means and how common it is. They cover metabolic syndrome criteria, variation across ethnic groups, and why early elevations in blood sugar should not be ignored.
- •Hallberg says over 50% of American adults have diabetes or prediabetes, and 88% are not in optimal metabolic health by NHANES metabolic syndrome criteria
- •Attia lists the metabolic syndrome criteria: blood pressure, fasting glucose, triglycerides, HDL, and waist circumference
- •Thresholds differ for Southeast Asians, and African Americans can have normal triglycerides and HDL despite insulin resistance
- •Hallberg tells physicians not to ignore any elevation in blood sugar, and Attia raises retinal imaging as a possible early screen
- 27:47 – 36:16
Fatty Acid Basics and What a Lipid Panel Measures
Attia introduces saturated, mono- and polyunsaturated fats and asks about the C16 fatty acid. Hallberg shares slides on saturated fat in triglycerides and de novo lipogenesis, and Attia explains how a lipid panel reflects VLDL triglycerides.
- •Saturated fats have no double bonds, monounsaturated one, and polyunsaturated two or more
- •Hallberg says saturated fat in triglycerides is assumed to reflect high saturated fat intake, but that is not necessarily true
- •Attia explains that fasting triglycerides mostly reflect triglyceride carried in VLDL
- •De novo lipogenesis exports liver fat via VLDL
- 36:16 – 48:06
Feeding Studies: Dietary Saturated Fat vs. Blood Saturated Fat
Hallberg walks through two feeding studies. In both, much higher saturated fat intake on low-carbohydrate diets did not raise saturated fat in the blood, while 16:1 palmitoleic acid rose with higher carbohydrate intake.
- •In the six-phase isocaloric feeding study, saturated fat intake fell from 84 g to 32 g as carbohydrate rose, yet blood saturated fat did not rise on the high-saturated-fat diet
- •Palmitoleic acid (16:1) rose significantly as carbohydrate increased
- •A 12-week calorie-restricted comparison found a larger drop in serum saturated fat on the low-carb, high-saturated-fat arm
- •Triglycerides fell about 50% on very low carbohydrate versus about 20% on low fat, and Hallberg ties the low-fat drop to calorie restriction
- 48:06 – 1:04:12
Palmitoleic Acid, SCD-1, and the Liver's Protective Role
Hallberg explains that palmitoleic acid (POA) is a product of the enzyme SCD-1, driven by carbohydrate and insulin signaling in the liver, and tracks with triglycerides. She and Attia agree that this conversion is likely the liver protecting the body by exporting fat as VLDL.
- •POA is made by stearoyl-CoA desaturase (SCD-1), an independent marker of high triglycerides and abdominal adiposity
- •Carbohydrate intake feeds a cascade through insulin and SREBP-1 that raises SCD-1 and VLDL
- •Attia offers a teleological view that the liver exports excess fat to protect itself, and Hallberg agrees completely
- •Hallberg says the process starts before weight gain, so obesity should be seen as a consequence of metabolic disease and without bias
- 1:04:12 – 1:10:42
POA as an Early Biomarker and Personalized Carbohydrate Tolerance
Attia asks about leading indicators ahead of A1C and whether POA works across populations. Hallberg describes the research gap, studies linking POA to later risk, and the idea of using POA to find an individual's carbohydrate threshold.
- •Attia notes that A1C flags trouble 10–20 years after early molecular warning signs, and his practice uses CGM in non-diabetics
- •Hallberg says there are no good trials in African American populations because research focuses on white, middle-class people
- •Studies of childhood POA and POA at age 50 versus CRP at 70 suggest it predicts later problems
- •Hallberg wonders whether POA could set a personal carbohydrate threshold so some patients need not stay very low carb
- 1:10:42 – 1:16:53
Beta Cell Reserve, Reintroducing Carbs, and the Risks of Insulin
Attia asks about patients who reintroduce carbohydrate after a long period of restriction. Hallberg points to beta cell reserve and says some patients eventually regain function. They discuss reduced insulin doses as a real health gain and her view of how insulin management is explained.
- •Hallberg says carbohydrate reintroduction depends on insulin reserve and functioning beta cells
- •Some patients stay on lower insulin for years and then come off, which suggests dormant beta cells may recover
- •Attia says moving from 100 to 20 units of insulin is a major improvement even if the patient stays on insulin
- •Hallberg argues patients should be told that people put on insulin are more likely to die on it
- 1:16:53 – 1:30:04
The June 2017 Diagnosis: Stage Four Lung Cancer
Attia turns to Hallberg's cancer and recalls the last time they met before her diagnosis. She describes losing the ability to speak, the emergency brain surgery, the discovery of multiple lung tumors, and her immediate thought of moving to Oregon.
- •Hallberg, a never-smoker who was very healthy, lost her ability to speak on June 30, 2017 and was taken to the hospital
- •Imaging showed a large brain tumor and multiple chest tumors, and she had urgent brain surgery the next day
- •She says her first reaction was to want to move to Oregon for physician-assisted suicide to spare her family
- •Attia notes 12–14% of lung cancer patients are non-smokers, and Hallberg says non-smoking lung cancer is rising in thin, athletic women, with no known reason
- •Her cancer has an EGFR exon 19 mutation, treatable with tyrosine kinase inhibitors that are not curative
- 1:30:04 – 1:36:30
Grief, Telling the Kids, and Choosing to Live
Hallberg describes the grief and denial of the first days, being honest with her children, and setting herself the goal of reaching 11 years. She identifies the moment on a plane to an Aspen fellowship session when she decided to live fully.
- •Her overwhelming grief centered on her children, who were 7, 12, and 14
- •She and her husband promised never to lie to the kids about her illness
- •She set a goal of 11 years, until her youngest graduates
- •Her son's reaction to joking about retiring and the plane ride to the Aspen session pushed her to choose to live
- •Her experience as a privileged patient deepened her focus on health equity
- 1:36:30 – 1:54:10
The Plan to Extend Survival: Surgery and Its Failure
Hallberg explains her reasoning for removing the primary tumor to reduce the risk of TKI resistance. Attia explains what mediastinal involvement meant for the surgery, and she recounts the surgery failing and the depression that followed.
- •TKIs typically work for only months to a couple of years before resistance develops, so she needed a way to reach 11 years
- •She sought removal of her six-centimeter primary tumor to lower the chance of resistance mutations
- •The TKI cleared her small lung tumors within weeks, and other brain tumors were treated with radiation
- •Attia explains that nodal disease in the mediastinum makes lung resection futile, and that is what the surgeon found
- •She woke up in distress, fell into depression, and still returned to work the month of her brain surgery
- 1:54:10 – 2:07:53
Refusing to Be a Sitting Duck: Rotating Aggressive Therapies
After a new brain tumor and a switch to osimertinib, Hallberg searched for physicians who would treat her aggressively. She describes a strategy of constantly changing therapies, including chemo, anti-estrogen drugs, and lung radiation, and reaching no evidence of disease.
- •She rejected the standard approach of waiting for the cancer to return
- •She found physicians who favored constantly changing treatments to beat mutations before they emerge
- •Her regimen included chemo, anti-estrogen therapy with palbociclib, low-dose cisplatin, and osimertinib throughout
- •Radiation to the primary tumor brought a painful bone complication, and she declined long-term opioids
- •By fall 2019 she had no evidence of disease
- 2:07:53 – 2:12:38
Gemzar Toxicity, Multi-Organ Failure, and Recurrence
On gemcitabine, Hallberg became severely ill and was admitted through a backdoor route after being sent home. She developed multi-organ failure and atypical hemolytic uremic syndrome, later traced to a genetic inability to break down the drug, and the cancer returned in September 2020.
- •She was sent home from chemo with severe pancytopenia, then admitted to the ICU after physician friends intervened
- •She had respiratory, liver, and kidney failure and was diagnosed with atypical hemolytic uremic syndrome
- •Pharmacogenetic testing showed a mutation that kept her from clearing Gemzar, so she received toxic doses
- •No one would put her back on chemo afterward, leaving her in sit-and-wait mode
- •The cancer recurred in her right upper lobe in September 2020
- 2:12:38 – 2:18:27
Delays, Costs, and Inequity in Cancer Care
Hallberg describes a four-month delay between recurrence and starting a clinical trial, even with her advocacy skills and resources. She argues the system loses momentum after recurrence, notes tens of thousands of dollars in out-of-pocket costs, and asks how many less-privileged patients die in such gaps.
- •Diagnosed with recurrence in mid-September, she did not start a clinical trial until December 30
- •She had to push hard for a biopsy with enough tissue for a genomics report
- •Other patients told her the same thing happens often after recurrence
- •Her out-of-pocket costs were tens of thousands of dollars, and she and Attia note cancer's link to bankruptcy
- •The delay left her with bronchial compression and breathlessness
- 2:18:27 – 2:29:53
Living with Terminal Cancer: Time, Anger, and Advocacy
Attia asks how Hallberg decides how to spend her time among family, diabetes work, and cancer advocacy. She says her children come first, that she turns anger into action through health equity work, and that she does not claim cancer gave her a better perspective. The episode closes with thanks and housekeeping.
- •Early on it was hard to be around her kids because they reminded her of what she would lose
- •She keeps her diabetes platform and sees health equity as spanning diabetes and cancer
- •She rejects a superwoman image: she is usually just okay and says she loved her life before cancer
- •Attia calls her an inspiration, and she says this was the first time she had told her story publicly
